Part III — The Cost We Don't See

Chapter 6

Fertility

Some environmental costs are easy to see.

Smoke in the air.

Plastic on a beach.

A contaminated river.

A chemical spill.

Others are quieter.

They unfold inside the body.

A couple tries to conceive and can't.

A pregnancy ends too soon.

A baby arrives early.

A reproductive hormone shifts.

A sperm count falls.

An egg does not mature normally.

None of these events automatically points to an environmental cause. Fertility is extraordinarily complex, influenced by age, genetics, health conditions, infection, nutrition, medications, anatomy, lifestyle, and chance.

But over the past several decades, scientists have increasingly asked another question:

Could the environment around us also be influencing our ability to reproduce?

The answer emerging from the research is not simple.

But it is increasingly difficult to dismiss.

A Signal in Sperm

One of the most widely discussed signals comes from sperm counts.

In 2022, researchers published an updated systematic review and meta-analysis examining sperm concentration and total sperm counts using data from 223 studies and semen samples collected between 1973 and 2018.

Among men not selected on the basis of fertility, average sperm concentration declined by approximately 51.6 percent between 1973 and 2018.[1]

The researchers also reported evidence that the rate of decline had accelerated after 2000.

That is a remarkable finding.

And understandably, it has generated dramatic headlines.

But sperm count is not the same thing as fertility.

A lower population average does not mean that half of men are infertile.

Individual fertility depends on multiple factors, including total sperm count, motility, morphology, reproductive health of both partners, timing, age, and many other variables.

There has also been scientific debate over how sperm-count studies are collected and interpreted.

Still, the geographic expansion of the newer analysis strengthened evidence that the downward trend was not limited to North America, Europe, Australia, and New Zealand.

Researchers found declines among men from South and Central America, Asia, and Africa as well.[1]

So the question becomes unavoidable:

Why?

Lifestyle factors have been proposed.

Obesity.

Smoking.

Alcohol.

Diet.

Heat.

Stress.

Delayed parenthood.

Certain medications.

Sedentary behavior.

And environmental chemicals.

There is almost certainly no single explanation.

But endocrine-disrupting chemicals have become one of the most intensely investigated possibilities.

The Endocrine System: The Body's Messaging Network

To understand why environmental chemicals might affect fertility, we first have to understand hormones.

Hormones are chemical messengers.

Tiny amounts of these molecules help regulate some of the most fundamental functions in the human body:

Growth.

Metabolism.

Thyroid function.

Stress response.

Sexual development.

Menstrual cycles.

Ovulation.

Sperm production.

Pregnancy.

Fetal development.

Hormones work partly by binding to receptors—almost like biological keys fitting into locks.

An endocrine-disrupting chemical, or EDC, is broadly defined as an outside chemical or mixture capable of interfering with some aspect of hormone action.[2]

Some can mimic natural hormones.

Some can block hormonal signals.

Some can alter the production or breakdown of hormones.

Others can affect hormone receptors, transport, or signaling pathways.

That is what makes endocrine disruption different from the traditional image of poisoning.

A substance does not necessarily have to destroy a cell to alter biology.

It may instead change a signal.

And during reproduction and development, signaling matters enormously.

Chemicals We Encounter Every Day

Endocrine-disrupting chemicals are not one single group.

They include chemicals or chemical families found in or associated with:

Plastics.

Food packaging.

Cosmetics.

Personal-care products.

Pesticides.

Flame retardants.

Industrial chemicals.

Certain contaminated foods and water supplies.

Among the most studied are:

Phthalates.

Bisphenols such as BPA.

PFAS.

Polychlorinated biphenyls, or PCBs.

PBDE flame retardants.

Certain pesticides.

Some of these substances are persistent and can remain in the environment or body for long periods.

Others, such as many phthalates and bisphenols, are eliminated relatively quickly but can still create what scientists sometimes call continuous or repeated exposure because we encounter them so frequently.

That distinction is important.

A chemical doesn't have to remain inside the body for twenty years if we are exposed to it again every day.

Male Fertility

Male reproduction is especially useful for studying environmental effects because sperm production is measurable.

Researchers can examine:

Sperm concentration.

Total sperm count.

Motility.

Morphology.

DNA integrity.

Hormone concentrations.

A 2021 review of endocrine-disrupting chemicals and fertility concluded that substantial evidence supports negative associations between male reproductive outcomes and exposure to several chemical classes, including phthalates, PCBs, PBDEs, certain pesticides, and other environmental contaminants.[3]

Research has associated some EDC exposures with poorer semen quality, changes in reproductive hormones, altered sperm motility, and other markers of male reproductive health.

That does not mean exposure to one plastic container or one pesticide causes infertility.

Human studies are rarely that simple.

People are exposed to mixtures.

Exposure varies over time.

Sperm quality itself fluctuates.

Diet, illness, fever, medications, smoking, heat, age, obesity, and other factors can influence semen parameters.

That makes environmental reproductive research extremely difficult.

But when human epidemiology, animal studies, laboratory research, and known hormonal mechanisms begin pointing in the same direction, the signal becomes harder to ignore.

Female Fertility Is Even Harder to Study

Female reproduction poses additional scientific challenges.

Women are born with a finite pool of oocytes.

Fertility changes strongly with age.

Cycles vary.

Hormone levels fluctuate throughout the month.

Endometriosis, polycystic ovary syndrome, fibroids, ovarian reserve, uterine health, tubal factors, immune function, partner fertility, and countless other variables affect reproductive outcomes.

Exposure studies therefore have enormous complexity.

Still, researchers have found associations between certain endocrine-disrupting chemicals and outcomes including ovarian reserve, reproductive hormone changes, fertility-treatment results, time to pregnancy, and reproductive disorders.[3][4]

The evidence is not equally strong for every chemical or every outcome.

For example, reviews have found stronger evidence for some male reproductive effects than for female fertility outcomes, partly because women historically have been studied less frequently in environmental reproductive research.[3]

That knowledge gap itself is significant.

For decades, medicine often treated fertility primarily as a woman's issue.

Environmental science increasingly reminds us that reproduction is a couple-level biological system.

The sperm matters.

The egg matters.

The placenta matters.

The uterine environment matters.

And both parents bring a lifetime of biological and environmental history to conception.

Pregnancy Is Not Just Nine Months

Pregnancy introduces an even more important concept:

timing.

In toxicology, dose matters.

But during development, when an exposure occurs can matter enormously too.

There are periods during fetal development when organs are forming, hormones are directing differentiation, and tissues are rapidly dividing.

A biological disturbance during one developmental window may have a very different effect from the same disturbance later.

The fetus is not simply a small adult.

It is a developing organism receiving signals that help determine how organs and systems are constructed.

The placenta, meanwhile, is not merely a passive wall between mother and fetus.

It is an active endocrine and metabolic organ.

It regulates nutrient transfer.

Produces hormones.

Participates in immune regulation.

Controls aspects of fetal growth.

Helps manage communication between maternal and fetal systems.

Research increasingly examines whether endocrine-disrupting chemicals can affect placental function, hormone signaling, gene expression, and other processes involved in fetal development.[5]

This is one reason pregnancy represents such an important period in environmental health.

The Placenta Is Not an Impenetrable Barrier

For years, many people imagined the placenta as a near-perfect filter.

It isn't.

Some environmental chemicals can cross the placenta or otherwise influence placental biology.

Researchers have detected environmental contaminants or their metabolites in maternal blood, placental tissue, cord blood, amniotic fluid, and other biological samples.

That does not mean everything a pregnant person encounters reaches the fetus at the same concentration.

It doesn't.

The placenta provides important protective functions.

But it is not an impenetrable shield.

And that matters because fetal endocrine systems are developing.

The fetus depends on extraordinarily precise biological signaling.

Environmental endocrine disruptors have therefore become a major area of research in reproductive medicine and developmental toxicology.

Developmental Programming

One of the most fascinating concepts in this field is called developmental programming.

The idea is that conditions during fetal and early-life development can influence health much later in life.

We already accept this concept in other contexts.

Maternal nutrition matters.

Alcohol exposure matters.

Smoking matters.

Certain medications matter.

Severe infections can matter.

The intrauterine environment matters.

Researchers are investigating whether some chemical exposures during development can similarly alter biological programming through hormone signaling, epigenetic mechanisms, placental function, or changes in organ development.[2][5]

This does not necessarily mean a chemical directly causes a disease decades later.

The relationship can be much subtler.

An exposure might influence how a system develops.

That alteration might change vulnerability.

Then genetics, diet, later exposures, stress, infection, or aging may interact with that vulnerability years afterward.

Once again, the bucket appears.

Except this time, part of the bucket may begin filling before birth.

Pregnancy Outcomes

The American College of Obstetricians and Gynecologists has concluded that growing evidence links prepregnancy and prenatal exposure to certain toxic environmental agents with reproductive and developmental outcomes.

These reported associations include:

Infertility.

Miscarriage.

Preterm birth.

Low birth weight.

Some developmental outcomes.

And other reproductive concerns.[6]

The language here matters.

Associated with is not the same as proven to cause.

Environmental studies rarely have the experimental control available in pharmaceutical trials.

We cannot intentionally expose pregnant women to suspected endocrine disruptors just to see what happens.

So much of the human evidence comes from observational research.

Researchers measure chemicals or metabolites in blood or urine.

They estimate exposure.

They follow pregnancies.

They compare outcomes.

Then they attempt to adjust statistically for other factors.

This provides valuable information.

But it also leaves uncertainty.

That is why stronger conclusions often come from combining multiple lines of evidence:

Human observational studies.

Animal studies.

Cellular research.

Mechanistic biology.

Exposure science.

Toxicology.

When those lines begin converging, our confidence increases.

Phthalates and Preterm Birth

One area in which evidence has become particularly concerning involves phthalates.

Phthalates are used in numerous products and materials, including certain plastics, personal-care products, building materials, and other consumer applications.

Because many phthalates are rapidly metabolized, researchers often measure their metabolites in urine as an indicator of recent exposure.

Large epidemiological studies have associated exposure to certain phthalates during pregnancy with shorter gestational duration and increased risk of preterm birth.[7]

Preterm birth matters enormously.

A baby born prematurely can face increased risk of respiratory problems, neurological complications, developmental difficulties, and other health challenges.

This doesn't mean every pregnant person exposed to phthalates will deliver prematurely.

Exposure is widespread.

Most exposed pregnancies do not end in preterm birth.

Environmental risk is usually probabilistic, not deterministic.

A risk factor changes odds.

It does not write destiny.

PFAS and Pregnancy

PFAS have also become an important reproductive-health research area.

As discussed earlier, PFAS are persistent chemicals used historically in numerous industrial and consumer applications.

Some can remain in the human body for years.

Studies have examined PFAS exposure in relation to:

Fertility.

Pregnancy-induced hypertension.

Birth weight.

Immune development.

Thyroid function.

Pregnancy duration.

Other maternal and fetal outcomes.

The evidence varies by compound and outcome, and researchers continue to work through differences in exposure levels, study populations, and methods.

But the broader lesson is important.

Pregnancy does not occur in isolation from the environment.

The reproductive system is part of the environment we carry into conception.

The DES Lesson

If anyone doubts that external chemicals can alter human reproductive development, history has already given us a powerful example.

Diethylstilbestrol, or DES, was a synthetic estrogen prescribed to millions of pregnant women during the twentieth century because physicians believed it could help prevent miscarriage and pregnancy complications.

It didn't.

Instead, daughters exposed to DES in utero were later found to have increased risk of a rare vaginal and cervical cancer, reproductive-tract abnormalities, infertility, pregnancy complications, and other problems.

Sons exposed prenatally also experienced reproductive effects.

The medication was eventually withdrawn from pregnancy use.

DES matters because it demonstrated something profound:

Hormonal disruption during development can have consequences that do not become apparent until years—or even decades—later.

The person exposed might not even be the mother taking the medication.

It could be the developing child.

The Endocrine Society frequently points to DES as one of the clearest human examples of developmental endocrine disruption.[2]

It changed the way scientists think about hormones and fetal development.

Tiny Doses and Hormones

Endocrine disruption also challenges a simple assumption many of us learned about toxins:

More exposure equals more effect.

That often remains true.

But hormones work naturally at very low concentrations.

And endocrine systems can sometimes demonstrate nonlinear dose-response relationships.

In other words, the relationship between dose and effect may not always form a perfectly straight line.

A chemical interacting with hormone receptors can behave differently at different concentrations.

That makes endocrine toxicology particularly complex.

It does not mean "one molecule is dangerous."

Nor does it invalidate the fundamental importance of dose.

It means that assessing hormonally active compounds sometimes requires more sophisticated models than traditional high-dose toxicology alone.

The Endocrine Society has emphasized this issue in its scientific statements on endocrine-disrupting chemicals.[2][8]

The Mixture Problem

Then we confront one of the largest scientific challenges of all.

We don't encounter one endocrine-disrupting chemical at a time.

A person may simultaneously have measurable exposures to:

PFAS.

Phthalates.

Bisphenols.

Pesticides.

Flame retardants.

Air pollutants.

Metals.

And dozens of other compounds.

Regulatory toxicology traditionally evaluates chemicals largely one by one.

Human life doesn't work that way.

Researchers increasingly study mixtures because chemicals can sometimes influence similar biological pathways.

But mixture science is enormously difficult.

Imagine trying to understand not merely the effect of ten substances, but every possible combination of ten substances at different doses across different developmental periods in people with different genetics.

That is the scientific challenge we face.

And it is one reason I am careful when discussing cumulative toxic burden.

We cannot simply add ten exposure measurements together and call the result someone's "toxicity."

Biology isn't arithmetic.

But neither can we pretend that simultaneous exposures never interact simply because studying them is difficult.

This is an area where science is still catching up with reality.

What About Long-Term Development?

Perhaps the most emotionally charged question involves children.

Could prenatal exposure influence neurological development, puberty, metabolism, fertility, or disease risk later in life?

For certain chemicals and outcomes, there is significant evidence.

For others, the science remains preliminary or inconsistent.

NIEHS identifies endocrine disruption as an important area of research involving reproductive development, metabolism, immune function, puberty, and other health outcomes.[9]

Research has associated prenatal exposure to certain environmental chemicals with differences in fetal growth, gestational age, reproductive development, immune responses, and neurodevelopmental measures.[5][6][9]

But developmental research is extraordinarily difficult.

Children are exposed to thousands of influences after birth.

Genetics matter.

Nutrition matters.

Education matters.

Home environment matters.

Infections matter.

Socioeconomic conditions matter.

Later exposures matter.

When a developmental difference appears at age eight or eighteen, determining exactly what role a prenatal environmental exposure played can be extremely challenging.

That uncertainty should not be hidden.

But it should not become an excuse to stop studying the question.

What the Research Does—and Does Not—Say

At this point, it is useful to separate several ideas.

The research does support that environmental chemicals can disrupt endocrine signaling.

The research does support that certain endocrine-disrupting chemicals can impair reproduction in experimental animals.

The research does support associations in humans between some chemical exposures and markers of male and female reproductive health.

The research does support concern about certain prenatal exposures and pregnancy outcomes.

The research does support the idea that fetal development represents a particularly sensitive window.

But the research does not support saying that modern environmental chemicals alone explain declining fertility.

It does not support assuming that everyone exposed to an endocrine disruptor will become infertile.

It does not allow us to assign a specific percentage of one person's infertility to plastics, pesticides, PFAS, or cosmetics without far more evidence.

And it does not mean reproduction is collapsing because of one villainous molecule.

What it tells us is more complicated—and perhaps more important.

The environment is one part of reproductive health.

It deserves a place at the table.

Infertility Is Not a Personal Failure

There is another reason this conversation matters.

Fertility problems often carry shame.

People blame themselves.

Women are told they waited too long.

Men can experience sperm abnormalities as a challenge to masculinity.

Couples silently wonder what they did wrong.

Environmental reproductive science offers a different perspective.

Our reproductive systems do not exist separately from the world around us.

They respond to age.

Illness.

Genetics.

Nutrition.

Stress.

Heat.

Medications.

Lifestyle.

And potentially environmental exposures.

Infertility is usually not the result of one bad choice.

It is often multifactorial.

Sometimes no cause is ever identified.

Recognizing environmental contributors should not create another opportunity for blame.

A pregnant woman should not be made to believe that using one cosmetic product, drinking from one plastic bottle, or eating one conventional strawberry harmed her baby.

That is neither scientifically justified nor humane.

Environmental health should shift responsibility upstream, toward safer products, better research, cleaner environments, and clearer public information—not create impossible expectations of perfect individual behavior.

Pregnancy Should Not Require a Chemistry Degree

This is where I find the current system frustrating.

We tell pregnant women to avoid environmental hazards.

But then we place them inside a world containing thousands of products whose ingredients and exposures may be difficult to understand.

The burden becomes:

Read every label.

Research every ingredient.

Replace every container.

Change every cosmetic.

Test every water source.

Avoid every pesticide.

Worry about every meal.

That isn't realistic.

Pregnancy is already filled with enough anxiety.

ACOG's approach is more reasonable: clinicians can help patients identify meaningful exposures, take an environmental history when appropriate, and reduce exposures known or reasonably suspected to pose reproductive risks.[6]

The goal should be risk reduction, not impossible purity.

Practical Reduction Without Panic

The strategies that make sense are often the same ones discussed throughout this book.

Avoid smoking and secondhand smoke.

Wash produce.

Eat a varied diet.

Use appropriate protective equipment around occupational chemicals.

Avoid unnecessary pesticide use.

Ventilate when using strong cleaning products.

Do not heat food unnecessarily in plastics not designed for that purpose.

Reduce reliance on fragranced products if they cause symptoms or if you simply prefer fewer unnecessary exposures.

Follow local advisories about contaminated water or fish.

If you are pregnant or trying to conceive and work around solvents, pesticides, heavy metals, or other hazardous substances, discuss those exposures with an occupational-health professional or obstetric clinician.

These actions will not guarantee fertility.

Nothing can.

But they can reduce unnecessary exposures without turning life into a toxicology experiment.

Maybe the Canary Begins Before Birth

The fertility research changed the canary metaphor for me again.

I had been thinking about the canary as the person who reacts first.

The person with the rash.

The headache.

The fainting.

The sensitivity.

But reproductive science raises a more unsettling possibility.

Sometimes the first signal may not be a symptom we can feel.

It may be a population trend.

A declining sperm count.

Increasing reproductive difficulty.

A shift in developmental timing.

A pregnancy outcome appearing more frequently in populations with particular exposures.

Those are harder signals to hear because no single person can feel them.

They emerge only when scientists step back and look at thousands—or millions—of people.

The individual canary tells us something may be happening in one body.

Epidemiology asks whether the flock is changing.

And that may be one of the most important forms of early warning we have.

Because if reproductive changes are partly influenced by environmental conditions, waiting until we can identify one perfect cause may mean waiting for certainty that science rarely provides.

The responsible path lies between panic and indifference.

Follow the evidence.

Acknowledge uncertainty.

Reduce exposures when reasonable.

Keep studying the unanswered questions.

And remember that fertility is not merely about whether one couple can become pregnant.

It is about something larger.

It is the biological bridge between generations.

What we encounter today may matter not only to the bodies living now—

but to the bodies that are still being built.

References

1. Levine, H., et al. Temporal trends in sperm count: a systematic review and meta-regression analysis of samples collected globally in the 20th and 21st centuries.Human Reproduction Update (2023). The analysis included 223 studies and found that mean sperm concentration among men unselected by fertility declined by approximately 51.6% between 1973 and 2018, with evidence suggesting an accelerated decline after 2000. (PubMed)

2. Endocrine Society. Endocrine-Disrupting Chemicals. Scientific Statements and 2025 Position Statement. Defines endocrine-disrupting chemicals as outside chemicals or mixtures capable of interfering with hormone action and reviews evidence concerning reproductive, metabolic, thyroid, neurodevelopmental, and other biological effects. (Endocrine Society)

3. Green, M. P., et al. Endocrine disrupting chemicals: Impacts on human fertility and fecundity during the peri-conception period. Environmental Research (2021). Reviews evidence relating environmental endocrine-disrupting chemicals to male and female reproductive hormones, gametes, time to pregnancy, and fertility outcomes and identifies both stronger associations and major remaining knowledge gaps. (PubMed)

4. Gaskins, A. J., & Chavarro, J. E. Female exposure to endocrine disrupting chemicals and fecundity: a review.Reviews human epidemiological evidence concerning BPA, phthalates, parabens, triclosan, ovarian reserve, ovulation, reproductive hormones, IVF outcomes, and time to pregnancy, while emphasizing inconsistencies in the human literature. (PubMed Central (PMC))

5. Padmanabhan, V., Song, W., & Puttabyatappa, M. Endocrine-Disrupting Chemicals and Pregnancy. Endocrine Reviews (2021). Reviews maternal and fetal EDC exposure, placental and hormonal mechanisms, pregnancy outcomes, developmental programming, and the potential for prenatal exposures to influence later health. (Endocrine Society)

6. American College of Obstetricians and Gynecologists. Reducing Prenatal Exposure to Toxic Environmental Agents. Committee Opinion No. 832, reaffirmed 2024. ACOG states that evidence links certain prepregnancy and prenatal environmental exposures with reproductive and developmental outcomes and recommends incorporating practical exposure reduction into reproductive care where appropriate. (ACOG)

7. Radke, E. G., et al. Phthalate exposure and female reproductive and developmental outcomes: a systematic review of the human epidemiological evidence.Environment International (2019). Systematically evaluates human evidence involving phthalates and outcomes including time to pregnancy, preterm birth, spontaneous abortion, and pubertal development. (PubMed)

8. Gore, A. C., et al. EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocrine Reviews (2015). Reviews high-quality evidence involving endocrine-disrupting chemicals and female reproduction, male reproduction, thyroid function, neurodevelopment, neuroendocrine systems, obesity, diabetes, and hormone-sensitive cancers. (Endocrine Society)

9. National Institute of Environmental Health Sciences. Endocrine Disruptors. Reviews mechanisms and research concerning endocrine-disrupting chemicals and reproductive, developmental, immune, metabolic, and other health outcomes, including research on PFAS, phthalates, DES, and related exposures. (NIEHS)

10. Endocrine Society. Impact of EDCs on Reproductive Systems. Reviews the hormonal mechanisms through which endocrine disruptors may alter reproductive biology and discusses evidence concerning sperm, female fertility, reproductive development, BPA, phthalates, flame retardants, pesticides, and the historical example of DES. (Endocrine Society)

11. Contemporary Review. Endocrine disrupting chemicals: translating mechanisms into perinatal risk assessment.(2025). Review of 52 epidemiological and experimental studies examining prenatal exposure to BPA, phthalates, PFAS, placental function, fetal growth, endocrine and epigenetic changes, and neonatal outcomes. (PubMed)

12. Systematic Review. Associations Between Endocrine-Disrupting Chemical Exposure and Fertility Outcomes: A Decade of Human Epidemiological Evidence.Reviews human studies published from 2014–2024 involving BPA and analogs, phthalates, parabens, PFAS, and persistent organic pollutants and reported associations with semen quality, ovarian reserve, reproductive hormone levels, infertility, and assisted-reproductive outcomes. (PubMed Central (PMC))

For Chapter 7, I’d make “Separating Evidence from Fear” the backbone of the chapter, not just the ending. Cancer and chronic disease are where environmental-health writing can most easily overreach. The stronger argument is that genetics, aging, screening, lifestyle, infections, and environmental exposures all matter—and the contribution differs dramatically by disease and exposure.

Chapter 7

Cancer and Chronic Disease

Cancer frightens us in a way few other diseases do.

Perhaps it is because almost everyone knows someone who has had it.

A parent.

A sibling.

A friend.

A coworker.

Perhaps it is because cancer can appear in someone who seemed perfectly healthy.

Or because when someone receives a diagnosis, one of the first questions is often impossible to answer:

Why me?

Was it genetics?

Something I ate?

Something I breathed?

Stress?

A chemical?

Bad luck?

Something in my water?

Something I did twenty years ago?

Usually, there is no single answer.

Cancer is not one disease. It is hundreds of diseases involving different tissues, mutations, exposures, hormones, infections, inherited susceptibilities, and biological pathways.

Chronic disease is even broader.

Cardiovascular disease.

Diabetes.

Autoimmune disorders.

Neurological disease.

Chronic respiratory disease.

Cancer.

These conditions now account for an enormous share of illness and death worldwide.

And as I learned more about environmental health, I became interested in a question that sits underneath this entire book:

How much of chronic disease is written in our genes—and how much is shaped by the world those genes live in?

The answer is not either/or.

It is both.

Cancer Begins With Biology, Not Morality

Cancer occurs when cells acquire changes that allow them to grow, survive, and spread in ways normal cells do not.

Those changes can arise for many reasons.

Some are inherited.

Some occur naturally as cells divide.

Some are influenced by aging.

Some result from infections.

Some are promoted by hormones.

And some are caused or encouraged by environmental and occupational exposures.

The National Cancer Institute estimates that inherited genetic changes play a major role in only about 5 to 10 percent of cancers.[1]

That does not mean the remaining cancers are caused by pollution.

It means most cancers arise through some combination of acquired mutations, aging, biological processes, lifestyle, infections, and environmental exposures rather than through a single inherited mutation.

That distinction is important.

Genes matter.

But genes are not destiny.

And environment matters.

But environment is much larger than the chemicals in our homes.

In cancer research, environment can include:

Tobacco smoke.

Ultraviolet radiation.

Alcohol.

Diet.

Obesity.

Physical activity.

Infections.

Air pollution.

Occupational exposures.

Ionizing radiation.

And specific chemicals.

Our bodies exist inside all of those environments simultaneously.

We Already Know the Environment Can Cause Cancer

The idea that environmental exposures can cause cancer is not controversial.

It is established science.

Tobacco smoke causes cancer.

Ultraviolet radiation from the sun causes skin cancer.

Radon causes lung cancer.

Asbestos causes mesothelioma and lung cancer.

Benzene causes leukemia.

Arsenic can cause several cancers.

Alcohol causes multiple cancers.

Certain infections—including HPV and hepatitis viruses—can cause cancer.

Outdoor air pollution has been classified as carcinogenic to humans by the International Agency for Research on Cancer.[2]

The U.S. National Toxicology Program maintains its Report on Carcinogens, identifying substances, mixtures, and exposure circumstances known or reasonably anticipated to cause cancer in humans.[3]

So the debate is not:

Can our environment cause cancer?

It can.

The difficult questions are:

Which exposures?

At what dose?

For how long?

During what stage of life?

In which people?

And:

How much of the disease burden do those exposures explain?

Those questions are much harder.

What Does "Carcinogen" Actually Mean?

The word carcinogen is frightening.

But it is frequently misunderstood.

Calling something a carcinogen describes its hazard—its capacity to cause cancer under some conditions.

It does not tell us the actual risk created by every exposure.

Consider sunlight.

Ultraviolet radiation is carcinogenic.

That does not mean stepping outside for five minutes guarantees skin cancer.

Alcohol is a Group 1 human carcinogen.

That does not mean every person who drinks alcohol will develop cancer.

Asbestos is carcinogenic.

But the risk faced by someone who worked around airborne asbestos fibers every day for thirty years is very different from that of someone who briefly walked past an intact asbestos-containing material.

This distinction between hazard and risk is essential.

Hazard asks:

Can this cause harm?

Risk asks:

How likely is harm under the conditions of this exposure?

Without that distinction, almost any discussion about environmental carcinogens can become terrifying.

With it, we can make rational decisions.

Breast Cancer: More Than Genetics

Breast cancer is an important example because it is extraordinarily common and biologically complex.

Age is one of its strongest risk factors.

Inherited mutations such as BRCA1 and BRCA2 can dramatically increase risk in some families.

Reproductive history matters.

Hormonal exposure matters.

Alcohol matters.

Body weight after menopause matters.

Physical activity matters.

Breast density matters.

But environmental exposures are also being investigated.

Researchers have studied compounds capable of affecting estrogen signaling, including certain endocrine-disrupting chemicals, as well as occupational exposures, air pollution, solvents, and other agents.

The National Institute of Environmental Health Sciences has supported extensive research examining environmental factors and breast-cancer risk, including through the Sister Study, which enrolled more than 50,000 women whose sisters had been diagnosed with breast cancer.[4]

Some findings have suggested associations involving air pollution, endocrine-active compounds, and other exposures.

But breast cancer illustrates why environmental epidemiology is so difficult.

A tumor diagnosed at fifty-five may have begun developing years earlier.

Relevant exposures may have occurred decades before diagnosis.

Puberty may matter.

Pregnancy may matter.

Menopause may matter.

A single blood or urine sample taken after diagnosis cannot necessarily reconstruct a lifetime of exposure.

That creates one of the greatest challenges in environmental cancer research:

The exposure and the disease may be separated by decades.

Windows of Susceptibility

The breast is not the same organ throughout life.

It changes during puberty.

Pregnancy.

Breastfeeding.

Menopause.

Researchers therefore study windows of susceptibility—periods during which environmental or hormonal exposures may have different biological consequences because tissue is undergoing rapid development or change.[5]

This concept appears throughout environmental health.

Timing matters.

An exposure during fetal development may have a different effect than the same exposure at age forty.

An exposure during puberty may matter differently from one after menopause.

That complicates the question we naturally want science to answer:

"Did this chemical cause my cancer?"

Often, science cannot answer that question for an individual.

It can tell us whether an exposure increases risk across populations.

It can identify mechanisms.

It can estimate relative risks.

It can identify vulnerable periods.

But individual cancer causation is usually much harder to prove.

That uncertainty can be frustrating.

It is also scientifically honest.

Colon Cancer and a Changing Generation

Colorectal cancer raises a different concern.

Overall colorectal-cancer mortality has fallen substantially over recent decades, in large part because of screening, removal of precancerous polyps, earlier detection, and improved treatment.

But another trend has attracted enormous attention:

Colorectal cancer has been increasing among younger adults.

The American Cancer Society reports that incidence has been rising in people younger than fifty-five, even while rates declined historically among older adults.[6]

That shift is one reason routine colorectal-cancer screening for average-risk adults now begins at age forty-five in the United States.[7]

Why are younger people developing a cancer traditionally associated with older age?

We don't fully know.

Researchers are investigating:

Obesity.

Diet.

Physical inactivity.

Metabolic disease.

Alcohol.

Changes in the gut microbiome.

Antibiotic exposure.

Ultra-processed foods.

Environmental exposures.

And combinations of these factors.

Again, the answer may not be one thing.

Cancer rarely gives us that simplicity.

Food, the Microbiome, and Colon Cancer

Colon cancer also brings us back to food.

There is convincing evidence that processed meat increases colorectal-cancer risk.

Alcohol is another established cancer risk.

Obesity and physical inactivity contribute as well.

Researchers are now examining whether features of modern diets—including high consumption of ultra-processed foods—may also contribute to colorectal-cancer risk.

Large observational studies have found associations between higher ultra-processed-food consumption and colorectal cancer, particularly in some populations.[8]

But the mechanism is not yet completely understood.

Is the risk attributable to obesity?

Low fiber?

High refined carbohydrate intake?

Food additives?

Processed meats?

Changes to the microbiome?

Packaging chemicals?

Something about the food matrix?

A combination?

Those are active scientific questions.

And this is where I have learned to become comfortable saying:

We don't know yet.

"We don't know" is not scientific failure.

It is often the beginning of good science.

The Immune System Turns Inward

Cancer is not the only chronic-disease category researchers are trying to understand.

Autoimmune diseases have also become increasingly visible.

In autoimmune disease, the immune system mistakenly attacks the body's own tissues.

There are more than eighty recognized autoimmune diseases, including:

Rheumatoid arthritis.

Lupus.

Multiple sclerosis.

Type 1 diabetes.

Celiac disease.

Hashimoto's thyroiditis.

Inflammatory bowel diseases.

Psoriasis.

Sjögren's disease.

And others.

Women are disproportionately affected by many autoimmune conditions.

Genetics clearly matter.

But genes alone cannot explain everything.

Identical twins can share the same genetic susceptibility while only one develops autoimmune disease.

That tells us something important:

Something beyond DNA influences whether susceptibility becomes disease.

Genes Load the Landscape; Environment Helps Shape the Outcome

Autoimmune research increasingly examines interactions among:

Genetics.

Infections.

Hormones.

Smoking.

Diet.

Microbiome.

Medications.

Occupational exposures.

Air pollution.

Silica.

Solvents.

And other environmental factors.

For some relationships, the evidence is strong.

Crystalline silica exposure, for example, has been associated with several systemic autoimmune diseases.

Smoking is a well-established risk factor for rheumatoid arthritis, particularly in genetically susceptible individuals.

Certain infections can trigger or contribute to autoimmune processes.

NIEHS has identified environmental contributions to autoimmune disease as an important area of research.[9]

But we should be careful.

The fact that environmental factors can contribute to autoimmune disease does not mean every autoimmune condition is caused by "toxins."

That word is used far too casually.

Autoimmunity involves complex interactions among genetic susceptibility, immune regulation, environmental triggers, and chance.

For many patients, we may never identify the trigger.

When the Brain Meets the Environment

Neurological disease raises perhaps even more difficult questions.

The brain is protected by the skull and by the blood-brain barrier.

But it is not isolated from the environment.

Lead is neurotoxic.

Mercury can be neurotoxic.

Certain pesticides can damage the nervous system at sufficient exposures.

Solvents can affect neurological function.

Air pollution is increasingly being studied in relation to neurological disease.

Researchers have investigated environmental contributions to:

Parkinson's disease.

Alzheimer's disease and other dementias.

Peripheral neuropathy.

Neurodevelopmental disorders.

Multiple sclerosis.

Amyotrophic lateral sclerosis.

And other conditions.

Some associations are much better established than others.

Parkinson's disease provides an important example.

Evidence accumulated over decades has linked certain pesticide exposures with increased Parkinson's risk, particularly among occupationally exposed populations, although Parkinson's itself is multifactorial and cannot generally be attributed to a single exposure in an individual.[10]

The relationship among genetics, aging, mitochondrial function, inflammation, pesticides, solvents, and other environmental factors continues to be investigated.

Once again:

The environment may alter risk.

It does not necessarily determine destiny.

Air Pollution Does More Than Affect the Lungs

One of the most important shifts in environmental medicine has been understanding that air pollution isn't simply a respiratory problem.

Fine particulate matter—PM2.5—can penetrate deep into the lungs.

Exposure is strongly associated with cardiovascular and respiratory disease.

Air pollution has also been classified as carcinogenic to humans, with sufficient evidence linking outdoor air pollution and particulate matter to lung cancer.[2]

Researchers are additionally investigating associations between long-term air-pollution exposure and neurological outcomes, including cognitive decline and dementia.[11]

This changes the way we think about breathing.

A particle enters through the lungs.

But its biological consequences may not remain confined there.

Inflammation and cardiovascular effects can influence systems throughout the body.

The body, again, refuses to respect medical specialties.

Why Does It Feel Like Everyone Is Sick?

This is one of the questions I hear most often.

Why does it seem like everyone has cancer?

Why does everyone seem to have an autoimmune disease?

Why are younger people getting chronic illnesses?

Why does everyone know someone with Long COVID?

Why are fertility problems so common?

Are we actually becoming sicker?

The answer depends entirely on the disease.

For some conditions, incidence really has increased.

For others, diagnosis has improved.

For others, people are living long enough to develop diseases that were less visible when life expectancy was shorter.

And for still others, the apparent increase reflects a combination of factors.

This is where statistics become essential.

Aging Changes the Numbers

Cancer is overwhelmingly associated with age.

As populations live longer, more people reach ages at which cancer becomes common.

That alone increases the absolute number of cancer diagnoses.

Population growth does too.

So headlines saying "cancer cases will increase dramatically by 2050" can be true without meaning that every individual's risk is skyrocketing.

The World Health Organization's International Agency for Research on Cancer projects substantial growth in the global number of new cancer cases by 2050, driven importantly by population aging and population growth, alongside changing exposure to risk factors.[12]

That context matters.

Raw numbers and individual risk are not the same thing.

Better Detection Can Look Like More Disease

Medicine is also much better at finding disease.

Mammography.

Colonoscopy.

CT scans.

MRI.

Genetic testing.

Blood tests.

Autoantibody testing.

Electronic medical records.

Improved diagnostic criteria.

Diseases that once went undiagnosed may now receive names.

That is progress.

But it can make prevalence appear to rise.

If ten people had a disease in 1980 and only three were diagnosed, while ten people have it today and nine are diagnosed, the medical record will show a dramatic increase even if the true disease rate has not changed.

This phenomenon—ascertainment—is one reason trend data require careful interpretation.

But Some Trends Cannot Be Explained Away

At the same time, we should not use better diagnosis and aging to dismiss every increase.

Young-onset colorectal cancer is rising.

Certain other cancers have increased among younger adults.

Obesity and metabolic disease have increased dramatically.

Some autoimmune diseases appear to be increasing.

Environmental exposures have changed.

Diet has changed.

Physical activity has changed.

Microbiomes may have changed.

People encounter synthetic chemicals that did not exist several generations ago.

Air pollution patterns have changed.

Our infectious history has changed.

Our medication use has changed.

Our built environments have changed.

Human biology is living inside a profoundly different world than it occupied even a century ago.

It is scientifically reasonable to ask what those changes mean.

What is not reasonable is to decide the answer before doing the research.

Correlation Is Where Investigation Begins

Suppose a community near an industrial site develops an unusual number of cancers.

That deserves investigation.

It does not automatically prove the industrial site caused them.

Suppose someone develops an autoimmune disease after a mold exposure.

The timing matters.

It deserves attention.

But timing alone cannot establish causation.

Suppose a person with high PFAS blood concentrations develops cancer.

PFAS may be relevant.

But the individual result cannot tell us by itself whether PFAS caused that cancer.

This is one of the hardest ideas in environmental health.

A compelling story is not necessarily causal evidence.

Human beings are pattern-finding creatures.

We desperately want the moment when everything makes sense.

I understand that impulse.

I spent years connecting the dots in my own health.

But there is a difference between finding a pattern worth investigating and proving the mechanism behind that pattern.

That line is where credibility lives.

The Dose Still Matters

One of the most damaging phrases in environmental-health discussions is:

"There is no safe level of chemicals."

It sounds protective.

But scientifically, it is meaningless without specifying the chemical.

Everything is chemical.

And dose remains one of the foundational concepts of toxicology.

Some substances can be tolerated at meaningful doses.

Others present concern at extremely low doses.

Some accumulate.

Some are rapidly eliminated.

Some damage DNA.

Some disrupt hormones.

Some irritate tissue.

Some become harmful only after metabolism.

Some pose little risk under normal exposure conditions.

The relevant question is always specific.

Which substance? Which dose? Which route? Which duration?

Even carcinogens differ.

Some cancer risks increase strongly with exposure.

Others increase only slightly.

Some have clear occupational histories.

Others remain suspected rather than proven human carcinogens.

Words such as carcinogen and toxin should begin the investigation.

They should not end it.

Relative Risk Can Sound Scarier Than Absolute Risk

Another concept every reader of health headlines should understand is the difference between relative risk and absolute risk.

Imagine that a particular exposure increases the risk of a disease by 50 percent.

That sounds enormous.

But suppose the original risk was two cases per 10,000 people.

A 50 percent relative increase would raise that to three cases per 10,000.

The relative increase is:

50 percent.

The absolute increase is:

1 additional case per 10,000 people.

Both statements are mathematically correct.

But emotionally, they sound completely different.

This does not mean relative risks should be ignored.

Small increases in risk can have enormous public-health consequences when millions of people are exposed.

But as individuals, we deserve to know both numbers whenever possible.

Fear grows in the space where context disappears.

Separating Evidence From Fear

This may be the most important section in this entire book.

Environmental health lives in uncomfortable territory.

On one side is dismissal:

"Everything is safe."

"The dose is too small to matter."

"Everyone else is fine."

"You're worrying too much."

On the other side is certainty without evidence:

"Everything causes cancer."

"Your shampoo is poisoning you."

"Plastic is killing us."

"Mold causes every chronic illness."

"If you detox enough, you won't get sick."

Neither extreme serves us.

The first can ignore legitimate environmental hazards.

The second turns uncertainty into fear.

I want a third path.

Evidence without complacency.

Precaution without panic.

Curiosity without conspiracy.

Personal experience without pretending anecdote is proof.

Science without pretending science already knows everything.

That is where I want this book to live.

What We Know

We know that certain environmental exposures cause cancer.

We know tobacco smoke, asbestos, radon, ultraviolet radiation, alcohol, benzene, arsenic, and some occupational exposures increase cancer risk.

We know environmental factors can influence immune function.

We know some environmental exposures are neurotoxic.

We know endocrine-disrupting chemicals can interfere with hormonal biology.

We know air pollution contributes substantially to disease.

We know genetics interact with environment.

We know timing, dose, duration, and susceptibility matter.

We also know that human beings are exposed to mixtures rather than isolated laboratory chemicals.

And we know our ability to measure exposure has advanced faster than our ability to understand the biological significance of every measurement.

Those are facts worth taking seriously.

What We Don't Know

We do not know the exact contribution of every environmental chemical to every chronic disease.

We do not know what every low-level chemical mixture does over seventy years.

We cannot determine the cause of most individual cancers.

We cannot assume every detected chemical is dangerous at the detected concentration.

We cannot assume every illness that follows an exposure was caused by that exposure.

We cannot assume natural substances are safe.

And we cannot assume synthetic substances are dangerous.

Most importantly:

Uncertainty is not evidence of safety.

But it is also not evidence of harm.

Uncertainty means exactly what it says.

We need more information.

The Precaution Question

So what should we do while science catches up?

I have come to believe in a practical version of precaution.

If an exposure is known to be harmful, reduce it.

Don't smoke.

Test homes for radon where appropriate.

Use sun protection.

Follow occupational safety rules.

Reduce unnecessary exposure to solvents, pesticides, and other hazardous chemicals.

Ventilate indoor spaces.

Address water damage.

Pay attention to drinking-water advisories.

Eat a varied, nutritious diet.

Exercise.

Maintain a healthy weight when possible.

Get recommended cancer screenings.

Vaccinate against cancer-causing infections such as HPV and hepatitis B when appropriate.

And when there is uncertainty about a chemical that serves little purpose in your life, it is reasonable to choose a lower-exposure alternative.

You don't have to prove something is poisoning you before deciding you don't need it.

But you also don't have to live terrified of everything you cannot pronounce.

The Canary Is Not a Diagnosis

By this point in my journey, I had become deeply attached to the canary metaphor.

But I also understood its limitation.

A canary tells you something deserves attention.

It does not tell you exactly what is wrong.

If the bird falls from its perch, you investigate the mine.

You measure the gases.

You examine the ventilation.

You look for the source.

You don't simply announce:

"The mine is toxic."

That is how I think about chronic disease now.

A rise in young-onset cancer is a signal.

Declining sperm counts are a signal.

A cluster of occupational illness is a signal.

An increase in a particular autoimmune condition may be a signal.

A person who repeatedly becomes symptomatic in one environment is a signal.

Signals deserve investigation.

But investigation is what transforms a signal into evidence.

And evidence is what should guide action.

The Cost We Don't See

The most frightening environmental hazards are not necessarily the ones that make us sick immediately.

Sometimes immediate toxicity is easier to understand.

Touch the stove.

Feel pain.

Move your hand.

Cause and effect are obvious.

Chronic disease operates differently.

An exposure may happen today.

A biological change may happen tomorrow.

Another exposure may occur next year.

Disease may not appear for decades.

By then, the original environment may be gone.

The building demolished.

The product reformulated.

The workplace closed.

The chemical banned.

The memory faded.

That long delay is one reason environmental disease is so difficult to prove.

It is also why prevention matters.

Not because every exposure becomes disease.

Most do not.

But because by the time some consequences become visible, the opportunity to prevent the original exposure may be long gone.

This is the cost we don't see.

Not a dramatic poisoning.

Not everyone collapsing at once.

But small changes in risk distributed across millions of people and decades of life.

One additional cancer here.

One neurological disease there.

One autoimmune condition.

One pregnancy complication.

One person whose genetics and exposures happened to intersect in exactly the wrong way.

No single case proves the larger story.

But populations can reveal what individuals cannot.

That is why we need epidemiology.

Toxicology.

Environmental monitoring.

Long-term studies.

Cancer registries.

Biomonitoring.

And people willing to notice patterns without exaggerating them.

The canary is valuable precisely because it warns us before everyone is affected.

But once the canary reacts, our responsibility is not to panic.

It is to measure.

To investigate.

To question.

To follow the evidence wherever it leads.

Because protecting ourselves from environmental disease requires two things that can be surprisingly difficult to hold at the same time:

We must take possible dangers seriously.

And we must be equally serious about proving what is actually dangerous.

That is how we separate evidence from fear.

And that is how we learn when the canary is truly warning us about the mine.

References

1. National Cancer Institute. The Genetics of Cancer. NCI explains that cancer results from genetic changes arising from inherited variants, environmental exposures, and errors occurring during cell division, and estimates that inherited harmful genetic changes play a major role in approximately 5–10% of cancers.
National Cancer Institute, National Institutes of Health.

2. International Agency for Research on Cancer. Outdoor Air Pollution a Leading Environmental Cause of Cancer Deaths. IARC classified outdoor air pollution as carcinogenic to humans (Group 1), with sufficient evidence that exposure causes lung cancer and a positive association with bladder cancer.
International Agency for Research on Cancer, World Health Organization.

3. National Toxicology Program. 15th Report on Carcinogens. U.S. Department of Health and Human Services. Identifies agents, substances, mixtures, and exposure circumstances known or reasonably anticipated to be human carcinogens.

4. National Institute of Environmental Health Sciences. Sister Study. A prospective study of more than 50,000 women examining environmental and familial factors associated with breast-cancer risk.
National Institutes of Health.

5. National Institute of Environmental Health Sciences. Breast Cancer and the Environment Research Program.Research examining environmental exposures during periods of breast development and other potential windows of susceptibility.

6. American Cancer Society. Colorectal Cancer Facts & Figures 2023–2025. Documents declining historical incidence among older adults alongside increasing colorectal-cancer incidence in younger populations.

7. U.S. Preventive Services Task Force. Screening for Colorectal Cancer. JAMA (2021). Recommends colorectal-cancer screening beginning at age 45 for average-risk adults and continuing through age 75, with individualized decisions for certain older adults.

8. Wang, L., et al. Association of ultra-processed food consumption with colorectal cancer risk among men and women: results from three prospective US cohort studies. BMJ (2022). Found higher ultra-processed-food consumption associated with increased colorectal-cancer risk among men, while associations varied by sex and food subgroup.

9. National Institute of Environmental Health Sciences. Autoimmune Diseases. Reviews research into genetic and environmental contributors to autoimmune disease, including smoking, crystalline silica, solvents, infections, and other environmental factors.

10. National Institute of Environmental Health Sciences. Parkinson's Disease. Reviews research into environmental contributors to Parkinson's disease, including pesticide exposures and interactions among environmental and genetic factors.

11. National Institute on Aging. Environmental Factors and Alzheimer's Disease and Related Dementias. Reviews research examining air pollution and other environmental exposures in relation to cognitive decline and dementia risk.

12. International Agency for Research on Cancer / World Health Organization. Global Cancer Burden Growing, Amidst Mounting Need for Services. IARC's Global Cancer Observatory estimates substantial growth in worldwide cancer cases by 2050, driven importantly by population growth and aging as well as changes in exposure to risk factors.

13. American Cancer Society. Cancer Facts & Figures 2026. Annual surveillance report describing current U.S. cancer incidence, mortality, trends, screening, and disparities.

14. National Cancer Institute. Cancer Causes and Prevention. Reviews established and suspected cancer risk factors including tobacco, alcohol, infectious agents, radiation, hormones, obesity, chronic inflammation, and environmental exposures.

15. World Health Organization. Cancer: Carcinogenicity of the Consumption of Red Meat and Processed Meat.Summarizes IARC's evaluation of processed meat as carcinogenic to humans based primarily on evidence for colorectal cancer and red meat as probably carcinogenic to humans.

16. National Institute of Environmental Health Sciences. Air Pollution and Your Health. Reviews health effects associated with particulate matter and other forms of air pollution, including cardiovascular, respiratory, cancer, and neurological research.

17. National Cancer Institute. Environmental Carcinogens and Cancer Risk. Reviews established environmental and occupational carcinogens and emphasizes that cancer risk depends on factors including exposure intensity, duration, route, individual susceptibility, and other risk factors.

Chapter 8

The Children

If adults are canaries, children may be something even more vulnerable.

They are still being built.

Their brains are developing.

Their lungs are growing.

Their immune systems are learning.

Their endocrine systems are changing.

Their organs are maturing.

Their bodies are smaller, but their exposure to the world can be proportionally greater.

Children breathe more air, drink more water, and eat more food relative to their body weight than adults. They spend more time on floors and closer to dust. They put their hands and objects into their mouths. Their skin can be more permeable. Their metabolic and detoxification systems are still developing. And there are critical windows during which an exposure may affect a developing system differently than the same exposure would affect a mature adult.[1] (US EPA)

That makes children's environmental health different.

Not because every child is fragile.

Children are remarkably resilient.

But resilience is not invulnerability.

And when we talk about the air, water, food, chemicals, infections, and products surrounding us, we have to remember that the body receiving those exposures may weigh thirty pounds instead of one hundred and fifty.

It may also be building a brain.

The Rise of the Allergic Child

Allergies have become part of childhood in a way that seems almost ordinary now.

Nut-free tables.

EpiPens at school.

Eczema creams.

Daily antihistamines.

Children who cannot eat eggs, milk, peanuts, tree nuts, wheat, or other foods without risking a reaction.

In 2024, nearly 30 percent of U.S. children had been diagnosed with at least one of three common allergic conditions: seasonal allergy, eczema, or food allergy. Approximately 20.6 percent had diagnosed seasonal allergies, 12.7 percent had eczema, and 5.3 percent had food allergies.[2] (CDC)

Those numbers do not tell us exactly how much allergy prevalence has increased over generations, because diagnostic practices and surveillance methods change.

But allergy and immune-mediated disease have clearly become major pediatric-health issues.

The harder question is:

Why?

There is no single explanation.

Genetics matter.

But our genes have not transformed radically in a few decades.

So researchers have looked increasingly at the environment surrounding those genes.

The Immune System Has to Learn the World

The immune system is not born knowing exactly what deserves attack.

It has to learn.

A child's immune system must distinguish between:

A dangerous pathogen.

A harmless food protein.

Pollen.

Dust.

A pet.

The child's own tissues.

Trillions of microorganisms living in and on the body.

That education begins before birth and continues throughout infancy and childhood.

The microbiome appears to play a role.

So do infections.

Diet.

Breastfeeding.

Antibiotic exposure.

Pets.

Farm environments.

Air pollution.

Tobacco smoke.

Allergens.

Genetics.

And perhaps numerous other environmental influences.

This has led scientists to theories such as the hygiene hypothesis and the broader old friends hypothesis, which propose that reduced or altered microbial exposures early in life may influence immune development.

The idea is not that children should live in dirty homes or be deliberately exposed to dangerous pathogens.

It is that the immune system evolved in constant conversation with the microbial world.

Modern life may have changed that conversation.

The Antibiotic Question

This part of the science became particularly interesting to me because of my own history.

I had many antibiotics growing up.

Antibiotics are among the most important medical advances in human history.

They save lives.

They prevent complications.

They treat bacterial infections that once killed children routinely.

But antibiotics also alter microbial communities.

A course of antibiotics does not necessarily affect only the organism causing an infection. It can temporarily change parts of the gut microbiome as well.

Researchers have therefore been studying whether repeated or early-life antibiotic exposure may be associated with later allergic or immune-related conditions.

Some studies have found associations between early antibiotic exposure and asthma, allergies, inflammatory bowel disease, obesity, and other outcomes.

But this is extremely difficult research to interpret.

Children who receive more antibiotics may also have more infections.

The infections themselves may influence later health.

Genetic susceptibility may make a child both more prone to infection and more prone to asthma.

This problem is called confounding by indication.

The medication and the disease that prompted the medication become difficult to separate.

So I would never argue that antibiotics caused my later health problems.

That would go far beyond the evidence.

But my history made me interested in a larger question:

What shapes immune development during childhood?

And how many small influences can accumulate before a system begins behaving differently?

Asthma: Genes Meet Air

Asthma is one of the clearest examples of genetics interacting with environment.

Asthma often runs in families.

But environmental triggers strongly influence whether symptoms appear and how severe they become.

Known asthma triggers include:

Air pollution.

Tobacco smoke.

Wildfire smoke.

Mold.

Dust mites.

Cockroaches.

Pets.

Pollen.

Respiratory infections.

Other indoor and outdoor pollutants.

NIEHS notes that mold, air pollution, pest allergens, tobacco smoke, and other exposures can trigger childhood asthma, and research has linked early-life air-pollution exposure with increased asthma incidence.[3] (NIEHS)

This is one of the reasons children's air deserves special attention.

A child's lungs are not finished.

The respiratory system continues developing throughout childhood.

A child also breathes more air relative to body weight than an adult.[1]

So when wildfire smoke fills a city, the child and adult standing beside each other do not necessarily receive an equivalent biological dose.

The child's body is smaller.

The lungs are developing.

Breathing rates are different.

And children often spend substantial time physically active outdoors.

Again:

Same environment. Different body.

The Indoor Childhood

Children also spend an enormous amount of time indoors.

Homes.

Daycare centers.

Schools.

Cars.

Gyms.

Bedrooms.

Classrooms.

Indoor air can contain:

Combustion products.

Fragrances.

Cleaning chemicals.

VOCs.

Dust.

Mold.

Pest allergens.

Particles carried in from outdoors.

Chemicals from flooring, furniture, electronics, and building materials.

EPA specifically identifies indoor mold, cleaning and fragranced products, combustion products, and resuspended household dust among potential exposure sources for young children.[1] (US EPA)

A toddler's world is also remarkably close to the floor.

Think about where household dust settles.

Now imagine crawling through it.

Then putting your hand in your mouth.

Adults rarely interact with an environment this way.

Children do it hundreds of times.

That changes exposure.

Why Children Are More Vulnerable

Children are not simply smaller adults.

This may be the most important scientific point in the chapter.

EPA describes several reasons they may be more vulnerable to environmental hazards.[1]

They eat more food per pound of body weight.

Drink more water.

Breathe more air.

Their brains are developing.

Their lungs are developing.

Their immune systems are maturing.

Their kidneys and liver do not always process substances in the same way as adult organs.

Their blood-brain barrier is still developing.

Their behavior brings them into contact with soil, floors, dust, toys, and other sources adults encounter differently.

And perhaps most importantly:

Development creates windows of susceptibility.

During fetal development and childhood, organs and systems undergo rapid change.

If a particular biological signal is disrupted during one of those periods, the same exposure may matter differently than it would years later.

This is the same concept we encountered in fertility and pregnancy.

Timing matters.

The Developing Brain

Nowhere is timing more important than in the brain.

Human brain development begins before birth and continues for decades.

Neurons form.

Move.

Connect.

Prune.

Myelinate.

Networks specialize.

Language emerges.

Attention develops.

Executive function matures.

Emotional regulation evolves.

The brain is not merely growing larger.

It is continuously organizing itself.

That makes developmental neurotoxicology particularly important.

We already know some environmental exposures can damage the developing nervous system.

Lead is perhaps the clearest example.

There is no identified safe blood lead level in children.

Lead exposure can impair cognitive development and affect behavior and learning.

High levels of mercury can damage the nervous system.

Certain severe pesticide exposures can cause neurological injury.

The question facing researchers today is what effects, if any, lower-level or combined environmental exposures may have during sensitive developmental periods.

That is much harder to answer.

Autism: What We Know and What We Must Not Claim

Autism deserves extraordinary care in any discussion of environmental health.

Autism spectrum disorder is a neurodevelopmental condition characterized by differences in social communication and interaction and by restricted or repetitive behaviors, interests, or patterns.

It is not a poisoning syndrome.

It is not something caused by poor parenting.

And it is not caused by vaccines.

NIEHS explicitly states that research has found no link between autism and vaccines, including vaccines containing thimerosal.[4] (NIEHS)

That point is not ambiguous.

Autism has a strong genetic component.

Researchers have identified numerous rare genetic variants, common genetic differences, chromosomal conditions, and inherited factors associated with autism.

But autism is also biologically heterogeneous.

There is probably no single pathway that explains every autistic person.

This is why researchers increasingly study gene-environment interaction.

Not:

"Which toxin causes autism?"

But:

"How might environmental and biological factors interact during neurodevelopment in susceptible individuals?"

That is a much more scientifically responsible question.

Are Autism Rates Really Rising?

The number of children identified with autism has increased dramatically.

CDC's latest surveillance estimate, based on 2022 data from sixteen U.S. communities, found that approximately 1 in 31 eight-year-old children had been identified with autism spectrum disorder.[5] (CDC)

In CDC surveillance data from 2000, the estimate was approximately 1 in 150.

That difference is enormous.

But those numbers cannot simply be interpreted as proof that environmental toxicity caused a massive increase in autism.

Several things have changed.

Diagnostic criteria broadened.

Awareness improved.

Children are evaluated earlier.

Girls and minority children who historically may have been overlooked are increasingly identified.

Access to developmental services changed.

Medical and educational records capture autism differently.

CDC itself notes substantial differences in autism identification across communities, suggesting that evaluation and diagnostic practices contribute significantly to observed prevalence.[6] (CDC)

It remains scientifically reasonable to investigate whether some part of the increase reflects changes beyond diagnosis and recognition.

But the surveillance numbers alone cannot tell us how much.

What Environmental Autism Research Actually Examines

Researchers are studying several prenatal and early-life factors associated with autism risk.

NIEHS identifies areas of investigation including:

Prenatal air pollution.

Certain pesticide exposures.

Parental age.

Prematurity.

Maternal metabolic conditions.

Maternal immune activation.

Certain pregnancy complications.

Genetic susceptibility interacting with environmental exposures.[4] (NIEHS)

Some studies have reported associations between prenatal exposure to air pollution or certain pesticides and increased likelihood of autism.

But association is not the same as causation.

These exposures do not explain most autism.

And even when a risk factor is statistically associated with autism, the overwhelming majority of exposed children may not develop autism.

This is the difference between risk factor and cause.

It is one of the most important distinctions in this book.

Autism Is Not Something to Blame on Mothers

Environmental-health discussions can become particularly harmful when pregnancy is involved.

A study finds an association.

A headline appears.

And suddenly mothers are wondering:

Was it because I lived near a road?

Because I used plastic?

Because I got sick while pregnant?

Because I took medication?

Because I ate the wrong thing?

That is not what the science says.

Autism is complex and strongly influenced by genetics and developmental biology.

No parent should interpret environmental research as proof that one ordinary choice caused their child's autism.

That is neither scientifically justified nor compassionate.

The purpose of environmental research should be prevention of modifiable population risks where evidence supports action.

It should not become retrospective blame.

ADHD: Another Increasing Diagnosis

ADHD creates many of the same interpretive challenges.

Attention-deficit/hyperactivity disorder is a neurodevelopmental disorder involving persistent patterns of inattention, hyperactivity, and/or impulsivity that interfere with functioning or development.

It also has a strong genetic component.

According to CDC data collected in 2024, approximately 7 million U.S. children ages three through seventeen—11.7 percent—had a current ADHD diagnosis.[7] (CDC)

Again, an increase in diagnosis does not automatically mean an equivalent increase in biological incidence.

Awareness has improved.

Diagnostic criteria have evolved.

More children receive evaluations.

Girls and children with predominantly inattentive symptoms may be identified more often than in the past.

Educational expectations have changed.

Access to care matters.

But researchers also investigate environmental factors.

Environment and ADHD

The best-established environmental neurodevelopmental hazards are not mysterious.

Lead exposure is associated with attention and behavioral problems.

Prenatal tobacco exposure has been associated with ADHD, although genetic and familial confounding complicates interpretation.

Researchers also examine:

Air pollution.

Pesticides.

Phthalates.

Flame retardants.

Bisphenols.

Prenatal stress.

Nutrition.

Prematurity.

Other pregnancy and early-life factors.

NIEHS reports research linking high exposure to certain PBDE flame retardants with neurodevelopmental outcomes that include ADHD-like symptoms, fine-motor difficulties, and lower cognitive measures.[3] (NIEHS)

But again, we should resist a simplistic conclusion.

ADHD is not "caused by toxins."

Its heritability is substantial.

Environmental factors may modify risk, expression, severity, or development in some children.

That is a different statement.

And it is the scientifically responsible one.

Neurodiversity and Disease Are Not the Same Conversation

There is also an important human dimension here.

Autism and ADHD are often discussed under the umbrella of neurodiversity.

Many autistic people and people with ADHD view their neurodevelopmental differences as part of who they are, not simply as diseases to be prevented or eliminated.

At the same time, some individuals experience profound disability and require substantial lifelong support.

Both realities deserve respect.

Environmental research into brain development should not be framed as an attempt to erase neurodivergent people.

Research can ask whether preventable exposures contribute to neurological injury or alter developmental risk while still respecting the dignity and identity of people who are autistic or have ADHD.

Those positions are not contradictory.

The Immune System and the Brain Talk to Each Other

One of the most fascinating developments in modern biology is the recognition that systems we once treated as separate are deeply connected.

The immune system communicates with the nervous system.

The gut communicates with the brain.

Hormones influence immune function.

Inflammation influences neural signaling.

The microbiome produces metabolites capable of interacting with the immune and nervous systems.

The placenta communicates with both maternal and fetal biology.

This does not mean every developmental condition is an immune disorder.

It does mean the old model of treating the brain as isolated from the body is increasingly outdated.

Researchers examining autism, ADHD, allergies, asthma, and autoimmune disease are often studying overlapping biological themes:

Immune signaling.

Inflammation.

Genetics.

Microbiome development.

Maternal health.

Environmental exposures.

Metabolism.

The fact that these systems interact does not prove they share a single cause.

But it does suggest that the body is far more interconnected than the specialties we created to study it.

The Allergy Puzzle

The rise of allergic disease may offer one of the clearest examples.

Why does one child's immune system recognize peanut protein as food while another's responds as though it were a dangerous invader?

Genetics matter.

Skin barrier function matters.

Early exposure may matter.

Microbiome development may matter.

Eczema is strongly associated with later food allergy in some children.

Timing of food introduction matters.

Environmental allergen exposure matters.

Research has changed pediatric advice as evidence changed.

For years, parents were sometimes advised to delay introduction of allergenic foods.

Then the landmark LEAP trial demonstrated that introducing peanut early to certain high-risk infants dramatically reduced development of peanut allergy compared with avoidance.

Science corrected itself.

That is worth celebrating.

It demonstrates something essential:

Good science is allowed to change its mind.

Immune Dysfunction Is Not One Diagnosis

The phrase immune dysfunction can also become vague very quickly.

It may refer to:

Allergy.

Autoimmunity.

Immune deficiency.

Chronic inflammation.

Abnormal mast-cell activity.

Altered immune responses to infection.

These are not interchangeable conditions.

An overactive allergic response is not the same as an immune deficiency.

Autoimmunity is not the same as MCAS.

Chronic inflammation is not automatically evidence of environmental toxicity.

Precision matters.

But there is a larger point:

The immune system develops in relationship with the environment.

NIEHS identifies children's immune systems as particularly vulnerable because they are still maturing, and early-life exposures may influence health in ways that appear immediately or years later.[1][3] (US EPA)

This makes childhood an especially important period for prevention.

Childhood Exposure Is Not Just a Smaller Adult Dose

Imagine an adult and a child drinking the same glass of contaminated water.

Same concentration.

Same volume.

But not the same dose per unit of body weight.

Now imagine the child drinks proportionally more water throughout the day.

Crawls through household dust.

Puts toys in their mouth.

Plays outside in soil.

Breathes faster.

Has developing kidneys.

A developing immune system.

A developing brain.

And may live another eighty years after the exposure.

This is why environmental standards sometimes include additional protections for children.

The issue isn't simply smaller bodies.

It is different biology + different behavior + longer time horizon.

Poverty Changes Exposure

Children's environmental risk is also not distributed equally.

A child does not choose their zip code.

Or their water system.

Or whether their family can afford an air purifier.

Or whether their school has adequate ventilation.

Or whether their apartment has mold.

Or whether a freeway runs beside their neighborhood.

Or whether their parents work in occupations that bring contaminants home on clothing.

Housing quality matters.

Neighborhood pollution matters.

Access to healthcare matters.

Nutrition matters.

Socioeconomic conditions can shape both exposure and resilience.

Environmental health therefore cannot be reduced entirely to shopping choices.

A family cannot purchase its way out of every exposure.

Sometimes the solution must be structural.

Cleaner air.

Safer housing.

Lead-free pipes.

Better schools.

Effective building codes.

Pollution controls.

Workplace protections.

Safe water.

Those are public-health interventions, not lifestyle trends.

We Must Be Careful With the Word "Epidemic"

When diagnoses increase, we often hear the word:

epidemic.

An autism epidemic.

An ADHD epidemic.

An allergy epidemic.

Sometimes the word reflects a real rise in disease.

Sometimes it reflects increasing diagnosis.

Sometimes both.

Calling every increase an epidemic before understanding why it occurred can create fear faster than science can provide context.

The correct questions are:

Did biological incidence increase?

Did diagnostic criteria change?

Did awareness increase?

Did access to healthcare improve?

Did recordkeeping change?

Did environmental exposures change?

Did survival improve?

Did demographics change?

Usually, more than one answer is involved.

Why One Child Reacts and Another Does Not

Children brought me back again to the central question of this book.

Why does one child develop asthma while a sibling doesn't?

Why does one develop eczema?

Why does one become allergic to peanuts?

Why does one exposed to pollution develop significant symptoms while another appears unaffected?

The answer may involve:

Genetics.

Timing.

Dose.

Previous illness.

Prenatal conditions.

Immune development.

Microbiome.

Nutrition.

Sex.

Age.

Social conditions.

Chance.

And exposures.

The canary principle does not mean the most sensitive child is defective.

It means variability is biology.

But here we have to add something else.

Children cannot advocate for themselves the way adults can.

They cannot necessarily identify a headache as an air-quality problem.

They cannot choose to move away from a contaminated neighborhood.

They cannot read a product label.

They cannot decide whether the school should remediate mold.

They depend on us to notice.

The Children's Canary

The old miners watched the bird because they knew it would respond before they did.

Children sometimes occupy a similar position in environmental health.

Asthma can reveal poor indoor air.

Elevated blood lead can reveal a housing hazard.

Repeated respiratory symptoms can lead investigators to dampness or mold.

Patterns across thousands of children can reveal associations adults might otherwise miss.

But we must never use children merely as detectors after the fact.

The goal is not to wait until they become sick enough to warn us.

The goal is to design environments with their vulnerability in mind from the beginning.

That means asking questions before harm becomes obvious.

What is in the air in the classroom?

What is in the drinking water?

Is there lead in the building?

Is the ventilation adequate?

Is moisture being addressed?

What pesticides are being used?

What are children exposed to where they sleep, learn, eat, and play?

Are those exposures necessary?

Can they reasonably be reduced?

Protect Without Terrifying

There is a danger in writing a chapter like this.

Parents already worry about everything.

Pregnancy introduces one list of things to fear.

Parenthood introduces a thousand more.

A book about environmental health should not convince parents that the world is poison and that every developmental difference is something they caused.

That would be cruel.

And scientifically wrong.

Most children exposed to everyday environmental chemicals will not develop autism.

Most will not develop ADHD because of a household product.

Most children living in conventional homes will grow, develop, learn, and thrive.

The goal is not purity.

The goal is reducing known and unnecessary risks.

Don't smoke around children.

Address lead hazards.

Remediate persistent water damage.

Improve ventilation.

Follow air-quality warnings during wildfire smoke events.

Wash produce.

Store pesticides securely and use them according to directions.

Avoid unnecessary chemical exposures where practical.

Give children nutritious food.

Let them play outside when environmental conditions are safe.

Vaccinate them according to medical guidance.

Allow them appropriate contact with the natural microbial world rather than attempting to sterilize every surface around them.

And when something seems wrong, pay attention.

Not because every symptom points to toxicity.

But because children's symptoms deserve investigation.

The Question Is Not Whether Children Are Fragile

They are not.

Children recover from extraordinary things.

They adapt.

Learn.

Grow.

Heal.

But resilience should never become an excuse for preventable exposure.

A child's developing body is building the biological foundation they may carry for the next eighty or ninety years.

The brain they will think with.

The lungs they will breathe with.

The immune system that will defend them.

The endocrine system that will regulate them.

The reproductive system that may one day create another generation.

The effects of childhood therefore cannot always be measured only in childhood.

Some consequences may appear decades later.[1]

This may be one of the most profound lessons of environmental health:

The absence of immediate symptoms does not always mean the absence of an effect.

And the presence of a diagnosis does not necessarily tell us what caused it.

We have to be able to hold both truths.

They Are Not Our Experiment

For much of modern history, humans introduced products into the environment first and asked some of the harder biological questions later.

Lead.

Asbestos.

PCBs.

DDT.

Certain flame retardants.

PFAS.

History contains examples where useful materials became widespread before their long-term consequences were fully understood.

That does not mean every new chemical will become the next lead.

It means we should learn from experience.

Children should not have to provide the epidemiological evidence that finally convinces us an avoidable exposure matters.

When evidence of harm is strong, we should act.

When evidence suggests plausible risk but remains incomplete, we should investigate carefully and reduce unnecessary exposure when doing so is practical.

When evidence shows no association, we should say that clearly too.

That is especially important with autism.

Vaccines do not cause autism.[4]

Repeating disproven claims diverts attention from the genetic and environmental research that actually deserves investment.

Fear sends us toward the wrong questions.

Evidence helps us ask better ones.

Listen Carefully to the Youngest Canaries

Children are the least responsible for the environments they inherit.

They didn't design the chemicals.

Build the freeway.

Choose the plumbing.

Approve the pesticide.

Select the school ventilation system.

Manufacture the plastic.

Create the wildfire smoke.

Or decide what compounds would persist in the environment for generations.

They inherited all of it.

Just as they inherited our genes.

Perhaps that is why children's environmental health belongs so centrally in this book.

They remind us that environmental exposure isn't simply about personal choice.

It is about stewardship.

The world we build becomes biology for the generation that follows us.

Not every allergy is caused by pollution.

Not every asthma case is environmental.

Autism is not a toxin diagnosis.

ADHD is not evidence of chemical poisoning.

And children's immune systems are influenced by far more than the products surrounding them.

But we also know that environmental conditions can influence respiratory health, neurological development, immune function, and lifelong disease risk.

Those two truths can coexist.

This is where we must remain:

Neither dismissive.

Nor afraid.

Curious.

Precise.

Protective.

Willing to act when the evidence is strong.

Willing to admit when it isn't.

Because children may be smaller than us.

But the consequences of what happens to them are much larger.

They carry today's environment into tomorrow.

And if there are canaries among us who deserve our attention before all others—

perhaps they are the children.

References

1. U.S. Environmental Protection Agency. Children's Unique Vulnerabilities to Environmental Hazards. EPA explains that children eat, drink, and breathe more relative to body weight than adults; have developing neurological, respiratory, metabolic, endocrine, and immune systems; engage in behaviors that can increase exposure; and pass through critical windows of susceptibility during which environmental exposures may have lasting effects. (US EPA)

2. National Center for Health Statistics, Centers for Disease Control and Prevention. Diagnosed Allergic Conditions in Children Ages 0–17: United States, 2024.NCHS Data Brief No. 546 (2026). In 2024, 29.5% of children had diagnosed seasonal allergy, eczema, or food allergy; 20.6% had seasonal allergies, 12.7% eczema, and 5.3% food allergy. (CDC)

3. National Institute of Environmental Health Sciences. Children's Environmental Health. Reviews children's enhanced susceptibility to environmental exposures and research involving asthma, air pollution, mold, neurodevelopment, flame retardants, and other childhood-health outcomes. (NIEHS)

4. National Institute of Environmental Health Sciences. Autism. Reviews genetic contributions and research into gene-environment interaction, prenatal air pollution, pesticides, maternal metabolic and immune factors, prematurity, and other potential autism risk modifiers. NIEHS states that no link has been found between autism and vaccines, including vaccines containing thimerosal. (NIEHS)

5. Centers for Disease Control and Prevention. Data and Statistics on Autism Spectrum Disorder. CDC's ADDM Network identified autism in approximately 1 in 31 eight-year-old children across 16 participating U.S. communities in 2022. (CDC)

6. Centers for Disease Control and Prevention. Autism Prevalence Varies Across U.S. Communities. CDC notes substantial variation in autism identification across surveillance sites and explains that differences in evaluation and testing practices likely contribute to observed prevalence differences. (CDC)

7. Centers for Disease Control and Prevention. Data on ADHD in Children. Based on 2024 National Survey of Children's Health data, an estimated 7 million U.S. children ages 3–17, or 11.7%, had a current ADHD diagnosis. (CDC)

8. National Institute of Environmental Health Sciences. Asthma. Reviews genetic and environmental contributors to asthma and research concerning traffic pollution, indoor exposures, immune function, and childhood respiratory health. (NIEHS)

9. National Institute of Environmental Health Sciences. Asthma and Allergies and Their Environmental Triggers.Reviews dust mites, mold, pets, cockroaches, pollen, and other environmental allergens capable of triggering allergic responses and asthma symptoms. (NIEHS)

10. National Institute of Environmental Health Sciences. Autism Research. Describes the CHARGE, MARBLES, and EARLI studies examining interactions among genetics, prenatal and early-life environmental exposures, maternal health, pesticides, air pollution, phthalates, and other factors potentially associated with autism risk. (NIEHS)

11. U.S. Environmental Protection Agency. Human Health Risk Assessment — Risk Assessment and Children.Reviews children's disproportionate exposure per unit of body weight, developing metabolic systems, hand-to-mouth behavior, and special vulnerability to hazards including air pollution, lead, contaminated water, and persistent chemicals. (US EPA)

12. U.S. Environmental Protection Agency. Protecting Children's Environmental Health. EPA resources and research addressing children's distinct environmental vulnerabilities across the places where they live, learn, and play. (US EPA)

13. National Institute of Environmental Health Sciences. Children's Health Research. NIEHS describes prenatal and childhood environmental-health research involving chemical, pollutant, nutritional, and behavioral exposures and notes that fetuses, infants, and children are particularly vulnerable because organ, immune, and metabolic systems are still developing. (NIEHS)