Environmental Impacts on Male Factor Infertility

Dr. Bethany Mattson, ND

Let’s not forget about the sperm! Although women have a wide variety of fertility related issues, male factor infertility attributes to about 35% of infertility cases. When considering preconception care and optimal fertility, environmental toxin exposure should be assessed for both parents due to implications in both sperm and egg quality. When evaluating a male partner, there are several causes of infertility to consider including pre-testicular, with hypothalamic or pituitary causes, testicular, with issues of spermatogenesis, and post-testicular, including ductal conditions. Up to 80% of male infertility issues arise from testicular causes with problems involving sperm production with decreased sperm quality as a leading cause. 

Both sperm health and male endocrine health can be greatly affected by chemicals and pollutants in the environment. Exposure to various toxins in the air, in patient’s houses, and in the workplace is unavoidable and the negative effects on fertility rates is reflected in the literature.  Environmental exposures to various toxins often have a chronic low-level effect on health and may not always be picked up by lab work and testing. Although not always obvious, environmental exposures could be a key reason why male sperm quality and quantity has been decreasing over time. 

Environmental toxins contain xenoestrogens, which are considered endocrine disrupting chemicals that can have profound effects on endocrine health. Xenoestrogens bind to estrogen receptors and can mimic estrogen activity in the body. Elevated estrogen can negatively impact male fertility as testicular cells contain estrogen receptors and increased estrogen can compromise sperm production. 

There are 3 key endocrine disrupting pollutants that have been linked to male infertility: Bisphenol A, phthalates, and heavy metals.

BPA:

Bisphenol A (BPA) is a synthetic compound and is found in many household and food items including canned foods, food packaging, and plastic objects such as toys. BPA is a known endocrine disruptor and affects androgen, thyroid, and glucocorticoid receptors with widespread detrimental effects on the endocrine and reproductive systems. The hypothalamic-pituitary-gonadal axis is the key regulator of male reproductive health and a balance between key endocrine hormones including gonadotropin-releasing hormone (GnRH), LH, and FSH, is needed for optimal fertility. BPA has been found to decrease GnRH levels, which in turn decreases LH production and therefore lower overall testosterone production. This disruption in hormonal activity can lead to altered spermatogenesis, sperm transport, and sperm storage. BPA has also been linked to decreased sperm concentration, decreased motility, abnormal morphology, and decreased total sperm count. 

*One 2015 study examined serum plasma and seminal fluid of 174 men and found that BPA levels were higher in infertile men compared to healthy controls. Additionally, BPA levels were higher in seminal fluid compared to plasma, indicating that BPA greatly affects the male reproductive system. 

Phthalates:

Another common environmental exposure is found in phthalates. Phthalates are synthetic chemicals that are commonly used as plasticizers in many commercial products. Phthalates increase plastic flexibility and are ubiquitous in the US population. Common sources of phthalates include food packaging, vinyl flooring, cologne, and deodorant. There are links between phthalate exposure and decreased androgenic activity, reproductive abnormalities, and decreased sperm count. Additionally, an association between phthalate exposure and hyperplasia, hypospadias, cryptorchidism, and malformation of the epididymis has been found. Phthalates may cause DNA damage to sperm and mitochondrial disruption leading to increased oxidative stress and production of reactive oxygen species in infertile men.

*A study from 2012 examined 150 men and measured phthalate exposure and semen quality including volume, concentration, and motility. A statistically significant relationship was found between the phthalate metabolite monobutyl phthalate (MBP) exposure and sperm concentration. There was also a correlation between the phthalate metabolite monoethyl phthalate (MEP) and sperm motility. An additional study found that phthalate exposure was related to DNA damage of sperm and a 20% reduction of fertility was observed. 

Heavy Metals: 

Exposure to heavy metals mainly come from environmental, dietary, and occupational sources.  Lead and cadmium are two heavy metals that have been consistently linked to male infertility due to their accumulation in male reproductive organs. Increased lead exposure has mainly been associated with lower sperm count. Possible mechanisms include detrimental effects on testicular function and hormone alterations. Lead has been found to suppress sperm creatine kinase, which lessens normal sperm metabolism.

Cadmium is another heavy metal that contributes to male infertility and is a known endocrine disruptor. Smoking and occupational exposure are two common sources of cadmium, but there are many other environmental sources including dietary, pollution, and contaminated water. As with many other heavy metals and environmental toxins, standard blood testing mainly demonstrates current active exposure to xenobiotics. Heavy metals can accumulate and cause chronic exposure, and seminal fluid testing may be more reflective of overall body burden. 

*One study examined the seminal fluid of infertile and fertile men and measured seminal cadmium levels and semen parameters including sperm concentration and motility. Statistically significantly higher cadmium levels were found in the infertile group of men, suggesting that cadmium toxicity may contribute to male infertility. Additionally, those with the highest levels of cadmium had both lower sperm count and motility. 

Treatment Starting Points:

As with all environmental exposure to xenobiotics, avoidance is the best practice for treatment. Additional treatment options include lifestyle modifications, detoxification, and supplementation with antioxidants. Patient education is key in achieving avoidance and changes in dietary and household items can make a large impact on reducing toxin load. Organic food and filtered water should be consumed as much as possible to limit exposure. Household products that contain plastics and solvents should be avoided. 

Detoxification is a powerful tool to utilize if a patient has a known exposure to toxins or heavy metals. Easy detoxification techniques for patients include eating cruciferous vegetables, utilizing N Acetyl Cysteine (NAC) and melatonin supplementation, and sweating though exercise or sauna use. The metabolism and biotransformation of toxins and heavy metals cause a high amount of oxidative stress on the body and the production of reactive oxygen species (ROS). Lab testing including the DUTCH hormone panel can help uncover clues about levels of oxidative stress, methylation activity, and reduced glutathione production. Supplementation with antioxidants can neutralize the detrimental effects of ROS and possibly increase semen quality. 

Environmental exposure to toxins and heavy metals are ubiquitous and may be a large contributing factor to rising infertility rates. Prioritizing male reproductive health including improving sperm quality can provide a beneficial starting place for couples experiencing male factor infertility.