While it is known that sperm aneuploidy contributes to early pregnancy losses and congenital abnormalities, causes are unknown and environmental contaminants are suspected.
Our goal was to evaluate associations between lifetime exposure to organochlorines, specifically dichlorodiphenyldicholorethylene (p,p’-DDE) and polychlorinated biphenyls (PCBs) and sperm aneuploidy in men from the general population of the Faroe Islands, a population with a known history of organochlorine exposures.
Serum and semen samples from men (n=90) ages 22-44 participating in Faroe Islands health studies were analyzed for p,p’-DDE and PCB (118, 138, 153, and 180) and adjusted for total lipids. Cord blood and age 14 serum were available for a subgroup (n=40) and also analyzed for p,p’-DDE and PCBs. Sperm fluorescence in situ hybridization (FISH) for chromosome X, Y, and 18 was used to determine rates of XX18, XY18, YY18 and total disomy. Multivariable adjusted Poisson models were used to estimate the relation between organochlorine exposure and sperm disomy outcomes.
Adult p,p’-DDE and total PCB serum concentrations were each associated with significantly increased rates of XX18, XY18 and total disomy. Age 14 p,p’-DDE and PCB concentrations were each associated with significantly increased rates of XX, XY and total disomy at adult age. Associations between cord blood concentrations of p,p’-DDE and PCBs and sperm disomy at adult age were not consistently significant.
Organochlorine exposures measured at age 14 and in adulthood were associated with sperm disomy in this sample of high exposure men, suggesting the impacts of persistent pollutants on testicular maturation and function need deeper investigation.
Sperm Aneuploidy in Faroese Men with Lifetime Exposure to Dichlorodiphenyldichloroethylene (DDE) and Polychlorinated Biphenyl (PCB) Pollutants, Environmental Health Perspectives; DOI:10.1289/ehp.1509779, 4 November 2015.
DDT in Pregnancy May Raise Breast Cancer Rates in Daughters
Women who were exposed to higher levels of the pesticide DDT in utero were nearly four times more likely to be diagnosed with breast cancer as adults than women who were exposed to lower levels before birth, according to a 54-year case-control study.
2015 Study Abstract
Currently no direct evidence links in utero dichlorodiphenyltrichloroethane (DDT) exposure to human breast cancer. However, in utero exposure to another xenoestrogen, diethylstilbestrol, predicts an increased breast cancer risk. If this finding extends to DDT, it could have far-reaching consequences. Many women were heavily exposed in utero during widespread DDT use in the 1960s. They are now reaching the age of heightened breast cancer risk. DDT exposure persists and use continues in Africa and Asia without clear knowledge of the consequences for the next generation.
In utero exposure to DDT is associated with an increased risk of breast cancer.
This was a case-control study nested in a prospective 54-year follow-up of 9300 daughters in the Child Health and Development Studies pregnancy cohort (n = 118 breast cancer cases, diagnosed by age 52 y and 354 controls matched on birth year).
Setting and Participants:
Kaiser Foundation Health Plan members who received obstetric care in Alameda County, California, from 1959 to 1967, and their adult daughters participated in the study.
Main Outcome Measure:
Daughters’ breast cancer diagnosed by age 52 years as of 2012 was measured.
Maternal o,p′-DDT predicted daughters’ breast cancer (odds ratio fourth quartile vs first = 3.7, 95% confidence interval 1.5–9.0). Mothers’ lipids, weight, race, age, and breast cancer history did not explain the findings.
This prospective human study links measured DDT exposure in utero to risk of breast cancer. Experimental studies are essential to confirm results and discover causal mechanisms. Findings support classification of DDT as an endocrine disruptor, a predictor of breast cancer, and a marker of high risk.
Sources and more information
DDT Exposure in Utero and Breast Cancer, The Journal of Clinical Endocrinology & Metabolism, doi/10.1210/jc.2015-1841, June 16, 2015.
Prenatal DDT exposure tied to nearly 4-fold increase in breast cancer risk, THE ENDOCRINE SOCIETY, eurekalert, 16-JUN-2015.
Prenatal DDT exposure linked to increased risk of breast cancer, medicalnewstoday, 17 June 2015.
Startling link between pregnant mother’s exposure to DDT and daughter’s risk of breast cancer, washingtonpost, June 17 2015.
In the late 1950s, Carson turned her attention to conservation, especially environmental problems that she believed were caused by synthetic pesticides.
Rachel Carson’s Silent Spring alerted a large audience to the environmental and human dangers of indiscriminate use of pesticides, spurring revolutionary changes in the laws affecting our air, land, and water. This Penguin Modern Classics edition includes an introduction by Lord Shackleton, a preface by World Wildlife Fund founder Julian Huxley, and an afterword by Carson’s biographer Linda Lear.
Rachel Carson (1907-64) wanted to be a writer for as long as she could remember. Her first book, Under the Sea Wind, appeared in 1941. Silent Spring, which alerted the world to the dangers of the misuse of pesticides, was published in 1962. Carson’s articles on natural history appeared in the Atlantic Monthly, the New Yorker, Reader’s Digest and Holiday. An ardent ecologist and preservationist, Carson warned against the dumping of atomic waste at sea and predicted global warming.
Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring
As they reached adulthood, female mice who were exposed in utero and just after birth to the pesticide DDT showed metabolic changes that put them at greater risk for obesity, type-2 diabetes, high cholesterol and related conditions in female offspring later in life, a study led by the University of California, Davis, says.
“Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring” is the first study to show that developmental exposure to DDT – like other persistent organic pollutants (POPs) – increases the risk of females later developing metabolic syndrome – a cluster of conditions that include increased body fat, blood glucose and cholesterol.
Dichlorodiphenyltrichloroethane (DDT) has been used extensively to control malaria, typhus, body lice and bubonic plague worldwide, until countries began restricting its use in the 1970s. Its use in malaria control continues in some countries according to recommendation by the World Health Organization. Individuals exposed to elevated levels of DDT and its metabolite dichlorodiphenyldichloroethylene (DDE) have an increased prevalence of diabetes and insulin resistance. Here we hypothesize that perinatal exposure to DDT disrupts metabolic programming leading to impaired metabolism in adult offspring. To test this, we administered DDT to C57BL/6J mice from gestational day 11.5 to postnatal day 5 and studied their metabolic phenotype at several ages up to nine months. Perinatal DDT exposure reduced core body temperature, impaired cold tolerance, decreased energy expenditure, and produced a transient early-life increase in body fat in female offspring. When challenged with a high fat diet for 12 weeks in adulthood, female offspring perinatally exposed to DDT developed glucose intolerance, hyperinsulinemia, dyslipidemia, and altered bile acid metabolism. Perinatal DDT exposure combined with high fat feeding in adulthood further impaired thermogenesis as evidenced by reductions in core temperature and in the expression of numerous RNA that promote thermogenesis and substrate utilization in the brown adipose tissue of adult female mice. These observations suggest that perinatal DDT exposure impairs thermogenesis and the metabolism of carbohydrates and lipids which may increase susceptibility to the metabolic syndrome in adult female offspring.
Neonicotinoids are the new DDT killing the natural world
Michigan yards songbirds are still being poisoned by DDT, a pesticide that was banned in the United States more than 40 years ago. Lethal concentrations were found in the birds’ brains, as well as in the worms they eat.
The stunning decline in bird numbers in North America and Europe are also being linked to a new generation of insecticides called neonicotinoids, a poison 5,000-10,000 times more toxic than DDT.
A recent study results suggest that the impact of neonicotinoids on the natural environment is even more substantial than has recently been reported and is reminiscent of the effects of persistent insecticides in the past. Future legislation should take into account the potential cascading effects of neonicotinoids on ecosystems.
Sources and More Information:
Songbirds dying from DDT in Michigan yards; Superfund site blamed, EnvironmentalHealthNews, dead-robins, July 28, 2014.
The ‘New DDT’ Is Starving Out Songbirds, MotherBoard, read, July 10, 2014.
Declines in insectivorous birds are associated with high neonicotinoid concentrations, Nature, doi:10.1038/nature13531, 09 July 2014.
Ancestral exposure to pesticides may cause adult onset kidney disease, ovarian disease and obesity in future generations
Implications for Obesity, Fertility, Disease
Washington State University researchers argues that exposure to the pesticide Methoxychlor – also known as Chemform, Methoxo, Metox or Moxie ; introduced in 1948 and widely used during the 1970s as a safer replacement for DDT – could cause diseases three generations later, in offspring who were never exposed to the chemicals themselves.
Most developed nations have banned the pesticide, which can behave like the hormone estrogen and profoundly affects the reproductive system. Methoxychlor was banned in the U.S. in 2003 but it is still widely used in Mexico and South American countries where the U.S. gets a significant portion of its produce.
Biologist Michael Skinner and his team found that if a rat fetus is exposed to the pesticide during the first trimester of pregnancy, the likelihood of kidney disease, ovary disease and obesity in their progeny was elevated for three generations. Multiple diseases were even more prevalent in the third generation – great-grandchildren – than in the second. This is called transgenerational epigenetic inheritance.
A variety of environmental toxicants have been shown to induce the epigenetic transgenerational inheritance of disease and phenotypic variation. The process involves exposure of a gestating female and the developing fetus to environmental factors that promote permanent alterations in the epigenetic programming of the germline. The molecular aspects of the phenomenon involve epigenetic modifications (epimutations) in the germline (e.g. sperm) that are transmitted to subsequent generations. The current study integrates previously described experimental epigenomic transgenerational data and web-based bioinformatic analyses to identify genomic features associated with these transgenerationally transmitted epimutations. A previously identified genomic feature associated with these epimutations is a low CpG density (<12/100bp). The current observations suggest the transgenerational differential DNA methylation regions (DMR) in sperm contain unique consensus DNA sequence motifs, zinc finger motifs and G-quadruplex sequences. Interaction of molecular factors with these sequences could alter chromatin structure and accessibility of proteins with DNA methyltransferases to alter de novo DNA methylation patterns. G-quadruplex regions can promote the opening of the chromatin that may influence the action of DNA methyltransferases, or factors interacting with them, for the establishment of epigenetic marks. Zinc finger binding factors can also promote this chromatin remodeling and influence the expression of non-coding RNA. The current study identified genomic features associated with sperm epimutations that may explain in part how these sites become susceptible for transgenerational programming.
Pesticide linked to three generations of disease, WSU, News, 24-Jul-2014.
Identification of Genomic Features in Environmentally Induced Epigenetic Transgenerational Inherited Sperm Epimutations, PLOS one, DOI: 10.1371/journal.pone.0100194, June 17, 2014.
Exposure to Pesticides When Pregnant Linked to 3 Generations of Disease, NewsWeek, pesticide-diseases, July 24, 2014.
Your Great Grandmother’s Exposure to Pesticides Could Be Making You Obese, Time, 3028766, July 25, 2014.