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Daily News Blog

10
Jul

Study Shows Brain Effects during Fetal Development Linked to Common Pesticide Exposure—Supports Call for Organic Alternatives

(Beyond Pesticides, July 10, 2020) A study published in June 2020 in Environmental Health journal is especially concerning for people who become, or plan to become, pregnant. It concludes that personal, agricultural, and household exposures to pesticides may increase the risk of a relatively rare fetal disorder called “holoprosencephaly.” The study finds that pre-conception and the first few weeks of pregnancy are the most vulnerable periods during which exposure can increase risk of this disorder, in which the embryo’s forebrain fails to develop into two distinct hemispheres. The study’s results reinforce Beyond Pesticide’s long-standing warnings of the dangers of pesticides to children and the necessity of shifting to a precautionary approach to the introduction and use of synthetic pesticides (and other chemicals) across all sectors. The importance of this shift is perhaps no more poignantly illustrated than in the impacts that pesticide exposure can have on new life.

The study, conducted from 2016 through 2019 by researchers from NIH (the U.S. National Institutes of Health) and the University of Wisconsin–Madison, is a case-control study — one that compares subjects who have a disease or disorder with “controls” who do not have the disorder, comparing the frequency of exposure to a particular risk factor in each group so as to determine the incidence relationship between the risk factor and the disease. In this research, the risk factor is pesticide exposure, and the disorder is holoprosencephaly (HPE).

The 91 subjects for the study were found through the National Human Genome Research Institute’s ongoing research projects on HPE. The 56 “controls” are children with Williams-Beuren Syndrome, a genetically caused disorder unrelated to HPE, but which is also characterized by congenital malformations (e.g., by pre- and post-natal growth delays, short stature, varying degrees of mental deficiency, and distinctive facial features). Subjects in both groups were predominantly from the U.S.

HPE is the most common malformation of the forebrain in humans, occurring in one of every 8,000 live births. The prognosis and lifespan of fetuses with HPE vary significantly, and depend to great extent on the severity of the abnormalities. Most do not survive even to birth; in less-severe cases, the brain may be more-nearly normal and those children may have a typical life expectancy, though the disorder is often accompanied by developmental delays. Many children born with holoprosencephaly have facial abnormalities (of eyes, nose, and lips), and some may exhibit endocrine dysfunction.

As with other congenital abnormalities, HPE’s etiology is complex and includes both genetic and environmental factors, which can interact to affect neurodevelopment. Only 25% of HPE cases exhibit mutations in one of the four genes most commonly associated with development of the condition. Other, non-genetic causes are thought to include environmental teratogens — agents that can cause malformations of an embryo. As the study authors write, “Epidemiologic and animal studies suggest that the interactions between genetic and environmental factors underlie the etiologic heterogeneity and complexity of human birth defects.” (A sample of congenital defects associated with pesticide exposure is available on Beyond Pesticides Pesticide-Induced Diseases: Birth/Fetal Defects website page.)

The researchers are interested in the relationship between pesticide exposures before and during pregnancy vis-à-vis HPE outcomes; no human studies to date had examined this relationship. The paper’s authors write, “Given the neurotoxic nature of many pesticides, increased susceptibility of the developing brain to toxic agents, associations of pesticides with brain malformations, and experimental evidence linking ingredients in pesticides with inhibition of the most important pathway in holoprosencephaly, investigation of pesticide exposure in HPE etiology is warranted.” [For science types: HPE brain and facial malformations “result from acute inhibition of the Sonic Hedgehog (Shh) pathway at a critical period of sensitivity during early embryogenesis.”]

Using a detailed questionnaire to estimate household, occupational, and environmental exposures to pesticide products (and other factors), the researchers examine maternal exposure to a number of pesticide compounds during four identified stages of pregnancy: preconception, early, mid, and late pregnancy. Among the pesticide categories surveyed are: personal insect repellents; lice or scabies medication; pet pest control products; insecticides for home or yard/garden use; and weed killers. The survey also asked about occupational exposures, and residential proximity to agricultural fields. Last, it sought information about some demographic characteristics, and about other factors that might either be protective or associated with HPE risk, such as maternal intake of folic acid before and during pregnancy, and substance use, including alcohol and nicotine, respectively.

Some highlights of the research findings include:

  • maternal use of folic acid supplements prior to conception and/or during the first month of pregnancy are associated with reduced odds of HPE
  • self-reports of pesticide use for some common pesticides, including those containing N, N-diethyl-meta-toluamide (DEET) are rare, but exposure to DEET-containing repellents during the preconception period are associated with increased risk for HPE; read about Beyond Pesticides DEET-related recommendations here
  • self-report of maternal exposure to any personal insect repellents in the preconception period are associated with increased odds for HPE
  • exposure rates for lice and scabies treatments are similarly low, and not associated with HPE risk
  • exposures to weed killers during preconception are not associated with HPE except where the exposures occur inside the home, in which case a trend toward association with HPE are found (researchers note that “residential pesticide use has been shown to contribute to the persistence of higher than recommended quantities of pesticide residues in the indoor air and [on] surfaces for as long as two weeks after a single application”)
  • residential proximity to an agricultural field (within 100 meters) during the preconception period or early pregnancy (i.e., the first trimester) are positively associated with HPE risk

Pesticide products used for pets or in the home show the strongest association with increased odds of HPE (compared to controls). Notably, exposures during pregnancy to insecticides and acaricides (compounds poisonous to ticks, fleas, and mites) used on pets, either via maternal use or use by another household member, are positively associated with risk for HPE. In addition, maternal exposure to personal insect repellents during preconception and/or during early pregnancy are positively associated with HPE — indeed, there is an observed twofold increase in risk.

The study authors assert that pesticides’ neurotoxicity is a likely actor in the compounds’ potential role as HPE teratogens. The study does not drill down to identify the specific active ingredients in the pesticides to which subjects reported exposure, nor does it examine dietary pesticide exposures. The authors note: “Future epidemiologic and experimental work should investigate associations between specific pesticide products and chemicals because nontargeted analyses grouping different pesticides including innocuous chemicals could mask the role of those chemicals contributing to HPE.”

The researchers identify five major pesticide classes — pyrethroids, neonicotinoids, carbamates, organochlorines, and organophosphates — and acknowledge a variety of modes of action across them re: developmental neurotoxicity. Given the recent relative increase of pyrethroid compound use in homes, and the strong associations between in-home pesticide and acaricide use, they say, “It would be especially imperative to examine possible associations between exposures to components of pyrethroid insecticide formulations and the risk for HPE.” They also assert that further investigations of genetic-plus-environmental interactions, as well as of biomarkers, are warranted.

The research does not establish causation, but rather, degrees of association between various kinds of pesticide exposure and subsequent incidence of HPE. The paper says, “Given the small sample size it is difficult to conclude causal associations, however, results of this analysis combined with emerging experimental data, increase potential weight of evidence that pesticide use and both active and inactive ingredients should be considered potential risk factors for HPE.” They also note that there is in vitro evidence that a co-ingredient in more than 1,000 pyrethroid insecticide products, piperonyl butoxide, inhibits the HPE-associated Shh pathway mentioned above.

Beyond Pesticides has written about the issue of pesticide exposure during critical developmental windows — which include the period prior to pregnancy and the first few weeks of the first trimester, especially. Those early weeks of pregnancy are when basic structures and systems such as the central nervous system (which includes the brain) develop rapidly. During these vulnerable developmental windows, neurodevelopmental toxins, such as those found in many active ingredients of pesticides, are particularly dangerous. Apart from development of HPE, some of the impacts and increased vulnerability that fetuses, babies, and children may endure may continue throughout childhood, putting kids at increased risk of cancer, developmental delays, and learning disabilities. Philippe Grandjean, MD, PhD, of Harvard’s T.H. Chan School of Public Health, has said, “Unfortunately, current testing paradigms do not properly assess the impact of risk factors during vulnerable exposure windows. Without new policies and guidelines, we cannot have a universal healthy start for children.”

In 2019, Dean Baker, MD, MPH — professor emeritus of medicine, epidemiology and public health in the School of Medicine, and former director of the Center for Occupational and Environmental Health, University of California Irvine, California — wrote for Beyond Pesticides’ journal, Pesticides and You: “There are millions of chemicals registered in the chemical registry of the American Chemical Society, or the Chemical Abstracts Service (CAS) Registry. There are over 80,000 chemicals that are produced and used in the United States, most of them having been synthesized in the past 50 years. There are 2,000 new chemicals introduced into commerce every year. The majority have not been tested for other than acute toxicity. Over 95% have not been tested for their effects to children.”

The pregnancy-related risks of HPE due to pesticide exposures to which this study points serve to illuminate the folly of the federal regulatory system’s attempts to “mitigate” risks of pesticide exposure through small and piecemeal rules. Given the many thousands of chemical pesticides on the market, the complexity of trying to ensure “relative” safety from them (especially considering potential synergistic interactions, as well as interactions with genetic and “lifestyle” factors), and the heaps of cash that fund corporate interests (i.e., selling these compounds) via lobbyists and trade associations, there is one conclusion. “Mitigation” of pesticide risks is a nibble around the edges of a pervasive poison problem; this approach does not at all adequately protect the fragility of life.

Many scientists have argued that approaches to the challenges posed by pests, weeds, fungal infections, disease-carrying insects, and other problems ought to be guided by the Precautionary Principle. Developed at a 1998 conference, the scientists that convened for it declared, in their Wingspread Statement on the Precautionary Principle: “When an activity raises threats of harm to human health or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically. In this context the proponent of an activity, rather than the public, should bear the burden of proof. The process of applying the precautionary principle must be open, informed and democratic and must include potentially affected parties. It must also involve an examination of the full range of alternatives, including no action.”

In application, this means that governmental regulation of any substance or activity proposed by an entity (usually a corporation) must require that proponents of the activity or substance, rather than the public, bear the burden of proof of safety. But more than 20 years hence, despite research results that support the eminent sense of this precautionary approach, and the advocacy of nongovernmental organizations and members of the public, the Precautionary Principle is still not the foundation of the U.S. approach to pesticides. Given the grossly inadequate nature of pesticide regulation in the U.S., the public cannot currently rely on governmental regulation, but must use local and personal actions to take precaution, as well as continue to advocate for federal, state, and locality precautionary paradigms.

For information on such personal precautions and protections, see these Beyond Pesticides’ website pages: Safer Choice: How to Avoid Hazardous Home, Garden, Community, and Food Use Pesticides; Center for Community Pesticide and Alternatives Information; Organic Agriculture, Eating with a Conscience, and Buying Organic Products; Mosquito Management and Insect-Borne Diseases; and Lawns and Landscapes, among others.

All unattributed positions and opinions in this piece are those of Beyond Pesticides.

Source: https://ehjournal.biomedcentral.com/articles/10.1186/s12940-020-00611-z

 

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