Flame Retardants and Pesticides Now Top Causes of IQ Loss

Summary: A long-term analysis found that exposure to flame retardants and pesticides accounted for most childhood intellectual disability cases linked to chemical exposure from 2001–2016, even as lead and mercury-related impacts declined.

Source: NYU

Overview

A study from NYU Grossman School of Medicine shows that adverse neurodevelopmental outcomes from early-life exposure to lead and mercury have declined in the United States, likely reflecting decades of regulatory limits on these heavy metals. However, the research also highlights a worrying shift: flame retardants and organophosphate pesticides now make up the majority of chemical-related cognitive harm in children.

Researchers report that estimated IQ loss attributable to the four chemicals they examined—poly brominated diphenyl ethers (PBDEs, used as flame retardants), organophosphate pesticides, lead, and methylmercury—fell from roughly 27 million IQ points in 2001–2002 to about 9 million IQ points in 2015–2016. Despite that overall decrease, PBDEs and organophosphate pesticides rose to represent a larger share of the remaining burden, growing from 67 percent to 81 percent of total cognitive loss over the same period.

“Our findings suggest that efforts to reduce exposure to heavy metals are paying off, but toxic exposures in general continue to pose a serious risk to Americans’ physical, mental, and economic health,” says lead investigator Abigail Gaylord, MPH, a doctoral candidate in the Department of Population Health at NYU Langone.

The study estimates that routine exposure to these substances between 2001 and 2016 affected approximately 1,190,230 children with some form of intellectual disability. The lifetime economic cost of those childhood exposures—measured as lost productivity and medical and societal expenses—is estimated at $7.5 trillion.

What the chemicals do

PBDEs, organophosphate pesticides, lead, and methylmercury are present in common items such as furniture upholstery, electronics, carpeting, and certain foods, including some seafood. These substances can accumulate in the body and interfere with organ systems. Lead and mercury have long been linked to disruption of brain and kidney function, while PBDEs and organophosphates can interfere with thyroid function and hormones essential to brain development. Early-life exposure can contribute to intellectual disability, learning difficulties, autism spectrum conditions, and behavioral disorders.

Lead author Leonardo Trasande, MD, MPP, emphasizes the financial as well as the human cost: “Although critics argue against costly regulations, unrestricted use of these chemicals is far more expensive in the long run, with American children bearing the largest burden.”

Study approach

The research, published in Molecular and Cellular Endocrinology, combined national biomonitoring data with established exposure–outcome relationships from prior environmental health studies. Investigators used blood measurements from women of childbearing age and five-year-old children from the National Health and Nutrition Examination Survey (NHANES) to estimate population-level exposures across 2001–2016. They then applied published dose–response estimates to calculate annual IQ points lost per unit of exposure for each chemical. The team translated lost IQ into economic impact using a lifetime value of $22,268 per lost IQ point and a cost estimate of $1,272,470 per case of intellectual disability.

PBDEs emerged as the single largest contributor to total intellectual disability burden in the analysis, accounting for a substantial share of IQ points lost and more than 738,000 estimated cases of intellectual disability across the study period. Lead, organophosphates, and methylmercury followed in their relative contribution.

Practical recommendations

Although regulatory restrictions have reduced exposures to some hazardous substances, the authors note that more limited action on flame retardants and pesticides appears to have shifted the risk landscape. Practical steps families can take to reduce exposure include increasing indoor ventilation to reduce persistent chemicals off-gassing from furniture and electronics, and choosing certified organic produce to lower pesticide intake. Trasande, who is chief of environmental pediatrics in the Department of Pediatrics at NYU Langone, stresses that these individual actions complement—but do not replace—stronger policy measures.

This shows a child playing with blocks
Among toxin-exposed children, the researchers found that the proportion of cognitive loss resulting from PBDE flame retardants and organophosphate pesticides increased from 67 percent to 81 percent during the study period. Image is in the public domain.

Limitations and next steps

The authors acknowledge that their estimates likely undercount the true impact of chemical exposures on neurodevelopment. Their analysis covered four major neurotoxicants but did not include the many other endocrine-disrupting chemicals now linked to developmental harm. They also note that adverse outcomes beyond IQ loss—such as behavioral problems and other health consequences—were not fully captured in the economic estimates. The team plans to expand this research by analyzing the cost of exposure to endocrine-disrupting chemicals in other countries and tracking trends as regulations and chemical use change.

Funding and authorship

Funding for the study was provided by National Institutes of Health grants RO1 ES022972 and RO1 ES029779. Key contributors from NYU Langone include Leonardo Trasande, MD, MPP; Abigail Gaylord, MPH; Akhgar Ghassabian, PhD; Julia Malits; and Teresa Attina, MD. Additional support came from Gwendolyn Osborne, MD, of the Office of Environmental Health Hazard Assessment in Oakland, California.

About this neurodevelopment research article

Original research: “Trends in neurodevelopmental disability burden due to early life chemical exposure in the USA from 2001 to 2016: A population-based disease burden and cost analysis.” Abigail Gaylord et al., Molecular and Cellular Endocrinology. DOI: 10.1016/j.mce.2019.110666.

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