Infertility Caused by Exposure to Organophosphate Pesticides and Neonicotinoids
DISCLAIMER: CONSULT WITH A DOCTOR BEFORE DECIDING ON A TREATMENT PLAN FOR ANY DISEASE OR INJURY.
Below, I discuss both organophosphates and neonicotinoids and their effects on fertility in men and women. Both organophosphates and neonicotinoids, as well as a slew of other pesticides and related chemicals (carbamates, organochlorines, pyrethroids, triazines, etc.), have been scientifically proven to decrease fertility as well as to negatively affect offspring after their birth. Some studies have even shown that exposure to these chemicals may affect the fertility of adolescent or adult individuals who were exposed to them in utero.
Infertility Due to Organophosphate Exposure
What are organophosphates?
Organophosphates are chemical insecticides that work as acetylcholinesterase inhibitors in the nervous system, as well as endocrine disruptors in the endocrine system. This means that, besides wreaking havoc on the nervous system, organophosphates cause also reproductive hormone imbalances, thyroid hormone imbalances, and disruption to all of the endocrine glands, which include the:
- Reproductive Organs
- Thyroid Gland
- Parathyroid Glands
- Adrenal Glands
- Pituitary Gland
- Pineal Gland
Infertility is a relatively common issue among couples trying to conceive, and there are many different factors that play a role in causing infertility, including exposure to toxic chemicals. Exposure to organophosphates, for example, has been associated with reproductive health problems including fertility issues in both men and women. While some sources may claim that organophosphates don’t affect fertility or reproductive health and that there’s no evidence to support this, there actually are numerous studies that have demonstrated that organophosphate exposure can negatively affect the fertility of both men and women (as well as the health of their unborn children).
Male Infertility and Organophosphate Exposure
Some of the scientifically proven effects of organophosphate exposure on male reproductive health include:
- Decreased testicular weight
- Decreased sperm motility
- Decreased serum testosterone levels
- Disruption of sperm production
- Degeneration of Sertoli cells in the testes (these cells are responsible for supporting sperm production)
- Decreased steroidogenesis
One study conducted in India observed that men who had been exposed regularly to pesticides (including organophosphates and/or carbamates) had decreased semen parameters in comparison to men who hadn’t been exposed to these pesticides. The men who sprayed pesticides on a regular basis demonstrated decreased sperm concentration, vitality, and morphology, as well as increased levels of luteinizing hormone and follicle stimulating hormone (though testosterone, prolactin, and thyroid hormones appeared to still be normal).
A different study in China observed the same results as the study above in male pesticide factory workers who had been interacting regularly with ethyl parathion and methamidophos. And, yet another study on agricultural workers in Mexico who had high levels of Dialkyl Phosphates (DAP) in their urine also demonstrated higher-than-usual levels of follicle stimulating hormone and luteinizing hormones like the men in the Iranian study. These findings all match each other, despite the different specific types of organophosphates/pesticides that the men were exposed to, and the fact that the studies were completed across three different countries. This fact, of course, makes the argument that organophosphate exposure negatively affects male fertility even more strong and compelling.
Female Infertility and Organophosphate Exposure
Studies have shown that organophosphate exposure in women can have the following effects on reproductive health:
- Decreased ovarian weight
- Decreased number of healthy, viable follicles
- Increased degeneration of existing follicles (such as is seen when a woman begins to get older)
- Interruption of estrus cycle
- Abnormal menstrual/reproductive cycle
- Decreased steroidogenesis
In animal studies done on rats, exposure to diazinon has been known to induce cell death in ovarian follicles, as has exposure to malathion. Female rats who had been exposed to quinalphos had a reduced number of healthy follicles, as well as a higher number of degenerating follicles and decreased myometrial thickness of the uterus.
Yet another study administered a combination of pesticides, including the organophosphate chlorpyrifos, to a group of female rats and their female offspring. The study noted that the mother rats who had been exposed to these pesticides were overall less likely to get pregnant, and that the pups of these females had a higher overall mortality rate (only 42% of the pups survived in the pesticide-exposed test group, in contrast with 76.4% of the pups in the control group). Additionally, the pesticide-exposed females tended to cannibalize their young, exhibited worsened metabolic parameters, and had an increase in liver weight.
The same study also followed the progress of the female offspring of these pesticide-exposed female rats (the female offspring were exposed to pesticides after birth as well, at the same dose as the mothers). In these offspring, numerous negative effects were observed, including a generally lower bodyweight than the control group counterparts (yet a higher rate of weight gain overall) and increased cecal weight, suggesting a difference in intestinal microbiota as well as in the health of the reproductive organs. In the reproductive organs themselves, the female offspring exhibited malformed ovaries with an atrophied appearance, and fewer corpora lutea per ovary. These rats also had notably reduced progesterone levels and increased proliferation of ovarian cells (which indicates a higher risk of ovarian and reproductive organ cancer) in comparison to the rats in the control group.
In humans, the effects of organophosphate exposure are also evident. In Iran, a study confirmed that exposure to organophosphates in females negatively affects hormone levels and reproductive organ structure (indicating not only general reproductive organ dysfunction, but also an increased potential for infertility). Another study in China supported these findings by observing that women who had higher levels of organophosphate and pyrethroid metabolites in their urine experienced a significantly longer time to pregnancy than the women with the lowest levels of these metabolites. Finally, as yet another example of how organophosphates affect human female fertility, the 2017 Environment and Reproductive Health (EARTH) cohort study demonstrated that high maternal exposure to pesticide residue on food is linked to an overall lower probability of achieving pregnancy and having a live birth in women receiving Assisted Reproductive Technology (ART) treatments.
Fetal, Infant, and Children’s Health Problems Due to Organophosphate Exposure In Utero
Some organophosphates have been shown to cause lower-than-average birth weights or higher mortality rates in newborns. They have also been associated with developmental issues and other negative outcomes in cases where the mother was exposed to organophosphates before or during her pregnancy.
Among some of the various risks to fetuses and children associated with maternal organophosphate exposure during pregnancy include:
- Abnormal primitive reflexes in newborns
- Mental and motor delays in preschool-age children
- Decreased visual and working memory
- Decreased verbal comprehension and processing speed
- Problems with perceptual reasoning
- Lower-than-average IQ scores among elementary school-age children
- Increased risk of developing autism spectrum disorder (ASD) or ADHD
- Arm tremors in children ages 7-11 years
Neonicotinoid Exposure and Infertility
What are Neonicotinoids?
Neonicotinoids are also known as Neonics. They are a class of neuro-active insecticides with a chemical similarity to nicotine. According to some sources, Shell and Bayer collaborated on the development of neonicotinoids in the 1980s (which raises the question… why is a petroleum company working with a pharmaceutical company at all? Aren’t these two things supposed to be completely separate? But I digress…). Though different from organophosphates, neonicotinoids deserve a special mention in this section about infertility due to their prevalence of use and negative effects on reproductive health. Note that particles containing these chemicals have been proven to travel nearly 330 feet away from the area where they were used.
Examples of neonicotinoids include:
Between 1999 and 2018, Imidacloprid had been the most widely used insecticide in the world. In 2018, the European Union made the decision to ban the outdoor use of this insecticide as well as that of clothianidin and thiamethoxam (two other widely used neonicotinoid insecticides). Unfortunately, France re-approved neonicotinoid use in 2018 for sugar beet production.
Some US states and Canadian have also restricted (though not completely banned) neonicotinoid use; for example, Ontario passed a law in 2016 intending to reduce neonicotinoid usage by 80%, and Minnesota’s 2016 law required that farmers obtain a permit to allow neonicotinoid use only in specific circumstances. However, none of these laws prohibit the use of neonicotinoids in seed coatings (an extremely common usage of these insecticides).
How do neonicotinoids affect fertility?
Neonicotinoid exposure affects both men and women, albeit in different ways. In general, imidacloprid exposure is linked to decreased liver and spleen size (note that the liver plays an important role in hormonal and reproductive health, which you can read more about here), though female reproductive organs have been shown to get smaller in many cases, though some studies suggest that the female reproductive organs could also sometimes get larger. Neonicotinoids affect men, too, and sperm quality has been shown to be reduced by chronic exposure to these chemicals.
One animal study observed that male rats who had been exposed to neonicotinoids (either in the form of imidacloprid or acetamiprid) didn’t have a significant difference in the number of oocytes that their spermatozoa were able to fertilize. However, eggs that had been fertilized with the neonicotinoid-exposed-sperm were approximately 20% less viable over time than the fertilized eggs in the control group.
Another animal study completed on white-tailed deer noted that fawns with the highest levels of imidacloprid in their spleens had the highest mortality rate; these fawns were born to mothers who had been exposed to imidacloprid in the water supply or via other sources. Female deer with higher levels of exposure to this particular neonicotinoid insecticide tended to have lower weight reproductive organs as well, indicating generally decreased fertility. In a rat study, female rats exposed to neonicotinoids experienced a decrease in ovarian size and an increase in uterine size.
Neonicotinoids in general have been noted to negatively alter estrogen production, as well as the activity of aromatase (an enzyme primarily responsible for the synthesis of estrogen) and CYP3A7 (another important enzyme thought to be essential for fetal and infant liver and organ development). Clothianidin exposure specifically during pregnancy and while breastfeeding has been linked to decreased serum 17-OH progesterone and corticosterone levels.
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