[OA] Pesticides and Human Reproduction
Pesticides and Human Reproduction
Reproductive injury is a dimension of pesticide toxicity that has come under increasing scrutiny. High-dose exposures to certain highly toxic, older-generation pesticides such as chlordecone (Kepone) and 1,2-dibromo-3-chloropropane (DBCP) were recognized decades ago to be capable of causing severe reproductive injury with infertility and azoospermia in occupationally exposed males. Direct injury to the gonads was the apparent mechanism. More recently, a range of sensitive and specific markers of reproductive function have been developed. These new markers allow sophisticated analyses of the effects of pesticides on reproduction at low exposure levels. Some of the recently recognized reproductive effects of pesticides reflect direct injury to the testes and ovaries. Others appear to be mediated through endocrine disruption by pesticide chemicals that can mimic or block the actions of naturally occurring hormones. DDT is an example of a potent endocrine disruptor that nearly caused extinction of the bald eagle and the osprey through interference with estrogen function.
The study in this issue of JAMA Internal Medicine by Chiu et al of the association between dietary pesticide exposure and decreased female fertility is an elegant example of a prospective epidemiological study that uses sophisticated biological markers to identify a subclinical effect of pesticide exposure on human health. In this study of women attending a fertility clinic, the authors found that regular consumption of conventionally grown, pesticide-treated fruits and vegetables was associated with increased risk of pregnancy loss, while consumption of organic fruits and vegetables significantly reduced risk of pregnancy loss and increased fertility. A range of potentially confounding factors was considered, and none changed the study outcome. All dietary pesticide levels were within the range of typical American exposure. Pesticide Residue Intake and Assisted Reproductive Technology Outcomes
What are the implications of this study?
It comes at a time when multiple lines of evidence suggest that human fertility is on the decline and that the frequency of reproductive impairment is increasing. Sperm counts in Western countries have fallen by 54% since 1973. The Centers for Disease Control and Prevention reports that incidence of hypospadias has more than doubled. Incidence of testicular cancer has increased by 55% in the United States since 1970. These changes are too rapid to be of genetic origin. They are clinically obvious findings, and thus improved diagnostic recognition is not a likely explanation. Environmental exposures are therefore almost certainly involved. To be sure, this study does not claim that pesticides actually caused increased rates of reproductive loss in women. Nor does it identify a specific pesticide or class of pesticides responsible for decreased female fertility.
The observations made in this study send a warning that our current laissez-faire attitude toward the regulation of pesticides is failing us. We can no longer afford to assume that new pesticides are harmless until they are definitively proven to cause injury to human health. We need to overcome the strident objections of the pesticide manufacturing industry, recognize the hidden costs of deregulation, and strengthen requirements for both premarket testing of new pesticides, as well as postmarketing surveillance of exposed populations—exactly as we do for another class of potent, biologically active molecules—drugs.
Pesticides and Human Reproduction
Reproductive injury is a dimension of pesticide toxicity that has come under increasing scrutiny. High-dose exposures to certain highly toxic, older-generation pesticides such as chlordecone (Kepone) and 1,2-dibromo-3-chloropropane (DBCP) were recognized decades ago to be capable of causing severe reproductive injury with infertility and azoospermia in occupationally exposed males. Direct injury to the gonads was the apparent mechanism. More recently, a range of sensitive and specific markers of reproductive function have been developed. These new markers allow sophisticated analyses of the effects of pesticides on reproduction at low exposure levels. Some of the recently recognized reproductive effects of pesticides reflect direct injury to the testes and ovaries. Others appear to be mediated through endocrine disruption by pesticide chemicals that can mimic or block the actions of naturally occurring hormones. DDT is an example of a potent endocrine disruptor that nearly caused extinction of the bald eagle and the osprey through interference with estrogen function.
The study in this issue of JAMA Internal Medicine by Chiu et al of the association between dietary pesticide exposure and decreased female fertility is an elegant example of a prospective epidemiological study that uses sophisticated biological markers to identify a subclinical effect of pesticide exposure on human health. In this study of women attending a fertility clinic, the authors found that regular consumption of conventionally grown, pesticide-treated fruits and vegetables was associated with increased risk of pregnancy loss, while consumption of organic fruits and vegetables significantly reduced risk of pregnancy loss and increased fertility. A range of potentially confounding factors was considered, and none changed the study outcome. All dietary pesticide levels were within the range of typical American exposure. Pesticide Residue Intake and Assisted Reproductive Technology Outcomes
What are the implications of this study?
It comes at a time when multiple lines of evidence suggest that human fertility is on the decline and that the frequency of reproductive impairment is increasing. Sperm counts in Western countries have fallen by 54% since 1973. The Centers for Disease Control and Prevention reports that incidence of hypospadias has more than doubled. Incidence of testicular cancer has increased by 55% in the United States since 1970. These changes are too rapid to be of genetic origin. They are clinically obvious findings, and thus improved diagnostic recognition is not a likely explanation. Environmental exposures are therefore almost certainly involved. To be sure, this study does not claim that pesticides actually caused increased rates of reproductive loss in women. Nor does it identify a specific pesticide or class of pesticides responsible for decreased female fertility.
The observations made in this study send a warning that our current laissez-faire attitude toward the regulation of pesticides is failing us. We can no longer afford to assume that new pesticides are harmless until they are definitively proven to cause injury to human health. We need to overcome the strident objections of the pesticide manufacturing industry, recognize the hidden costs of deregulation, and strengthen requirements for both premarket testing of new pesticides, as well as postmarketing surveillance of exposed populations—exactly as we do for another class of potent, biologically active molecules—drugs.
