The Importance of Pesticides Effects on Human Reproduction in Farmers
Habib Shojaei Saadi
May 04, 2012; Accepted: May 07, 2012;
Published: September 06, 2012
Pesticides are chemicals commonly used in homes and current agronomy to eradicate or keep away pests or halt their reproduction. Diverse series of chemicals such as insecticides, fungicides, rodenticides, pediculicides and biocides are subcategories within this category of chemicals.
Contact to pesticides can be through inhalation of contaminated air, ingestion
of food residues or/and contaminated water, dermal contact or across the placenta.
Most of the pesticides are readily accessible to the human body as they are
persistent and remain intact for long periods of time. According to the latest
Stockholm Convention on Persistent Organic Pollutants, 16 out of 22 the most
hazardous and persistent chemicals are pesticides. Henceforth, these truths
have made a mounting distress about the safety of pesticides and human health
Health risks that are associated with human pesticide exposure are cancer,
adverse effects on immune systems, neurodevelopment dysfunction, metabolic diseases
such as diabetes, endocrine system disruption and infertility (Gilden
et al., 2010; Rahimi and Abdollahi, 2007).
Pesticides also may cause difficulty in breathing, headaches, neurological or
psychological effects, irritation of skin and mucous membranes and skin disorders.
Dose, timing and duration of exposure are critical to the ability of a pesticide
to cause harmful effects.
The adverse effects of pesticides on human reproduction has been documented
more than 30 years ago (Whorton et al., 1977).
Although, most of the studies that have been conducted in human and animals
showed the potential reproductive health risks of pesticides exposure but there
is still essential to screen adverse reproductive outcomes of pesticides exposure
Pesticides may influence their adverse effects on reproduction on selected
stages of development including prenatal stage, prepubertal stage or the adult,
resulting in damage to the reproductive organs and/or impaired fertility (Malik
et al., 2011). They may directly make their action as (1) a reactive
chemical and cause germ cell damage (e.g., alkylating agents) or (2) taking
structural similarity to endogenous molecules, e.g., hormone agonists/antagonists.
Pesticide also may indirectly act and interrupt reproduction (1) by metabolism
to a direct-acting compound or reactive intermediate, (2) via endocrine alterations
such as increased/decreased steroid clearance or (3) by stimulating or inhibiting
neuroendocrine responses at the level of the thyroid, hypothalamus or pituitary
(Iyer and Makris, 2010).
In case of male reproduction, pesticides may act through hormonal or genotoxic
pathways (Shadnia et al., 2005). They may penetrate
the blood-testis barrier to potentially affect spermatogenesis, either by affecting
genetic integrity or hormone production (Perry, 2008)
leading to poor semen quality and reduced male fertility (Roeleveld
and Bretveld, 2008). In female, they may disrupt the hormonal function of
the female reproductive system and in particular the ovarian cycle may result
in modulation of hormone concentrations, ovarian cycle irregularities and impaired
fertility. Epidemiological studies on females showed that exposure to pesticides
has been associated with menstrual cycle disturbances, reduced fertility, prolonged
time-to-pregnancy, spontaneous abortion, stillbirths and developmental defects
which may or may not be due to disruption of the female hormonal function (Bretveld
et al., 2006).
Exposure to pesticides may occur by virtue of occupational or environments.
It has been shown that occupational exposures to pesticides adversely influence
male and female fertility (Bian et al., 2004;
Bretveld et al., 2006; Snijder
et al., 2012). Agricultural and horticultural occupations are of
importance as it has been shown that occupational exposure to pesticides in
these cases appears to consistently reduce fertility and/or fecundability (Mendola
et al., 2008).
Some of the epidemiological studies showed that employment in agriculture for
men increases the risk of specific morphological abnormalities in sperm, including
the decreased sperm count per ejaculate and declined percentage of viable sperm
(Hanke and Jurewicz, 2004) and spermatozoa DNA damage
(Bian et al., 2004). In addition, two studies
amongst cotton field workers in India reported increased male infertility, negative
pregnancy outcome and higher rates of abortions in their wives (Rita
et al., 1987; Rupa et al., 1991).
In women, agricultural pesticides exposure may affect menstrual cycles (Farr
et al., 2004) and may cause spontaneous abortions, congenital defects,
pre-maturity, delay in conception and infertility (Figa-Talamanca,
2006). Moreover, studies suggested that parental employment in agriculture
exposed to pesticides could decrease fecundability ratio and increase the risk
of congenital malformations in the offsprings (Hanke and
This is more severe in developing countries, in particular, that high exposure
to pesticides due to overused and misused of pesticides by farmers have been
reported (Wilson and Tisdell, 2001; Tariq
et al., 2007; Panuwet et al., 2012).
Therefore, it would be rational to conclude that in less developed countries,
farmers due to occupational exposure (Antle et al.,
1998; Tariq et al., 2007) and the people
living in rural areas due to environmental contamination exposure (Panuwet
et al., 2012) are at higher risk for acute and chronic health effects
associated with pesticides (Figa-Talamanca et al.,
2001; Atreya, 2008). In this regard, adverse effects
on human reproduction could be one of the consequences which several studies
showed male and female reproductive issues in farmers from developing/less developed
countries (Rita et al., 1987; Rupa
et al., 1991; Antle et al., 1998; Tariq
et al., 2007; Atreya, 2008; Panuwet
et al., 2012).
Showing the importance of the concern, recently the contribution of exposure
to pesticides and incidence of human diabetes has been bolded, an issue that
is going to be one of the global health dilemmas (Mostafalou
and Abdollahi, 2012). In fact, pesticides by their major toxicity as inducers
of free radical damage inside the whole body can disrupt many organs or defect
their function (Abdollahi et al., 2004). All together,
occupational exposures to pesticides particularly agricultural and horticultural
occupations appear to have serious adverse effects on male and female reproduction.
Farmers, especially those from less developed countries are in high exposure
to pesticides and subsequently more chance for potential pesticides human reproductive
issues. Therefore, a great need to increase awareness and education to safe
use for the workers and farmers who are occupationally exposed to pesticides
are essential. Furthermore, more epidemiological studies should be conducted
to elucidate the occupational exposure adverse effects of pesticides on human
reproduction in particular farmers from less developed countries. At the moment
nobody can claim that there is no link between pesticides exposure and reproductive
toxicity but yet it is impossible to state how many of human infertilities are
due to pesticide exposure.
Abdollahi, M., A. Ranjbar, S. Shadnia, S. Nikfar and A. Rezaie, 2004. Pesticides and oxidative stress: A review. Med. Sci. Monit., 10: RA141-RA147.
PubMed | Direct Link |
Antle, J.M., D.C. Cole and C.C. Crissman, 1998. Further evidence on pesticides, productivity and farmer health: Potato production in ecuador. Agric. Econ., 18: 199-207.
Direct Link |
Atreya, K., 2008. Health costs from short-term exposure to pesticides in Nepal. Social Sci. Med., 67: 511-519.
Bian, Q., L.C. Xu, S.L. Wang, Y.K. Xia and L.F. Tan et al., 2004. Study on the relation between occupational fenvalerate exposure and spermatozoa DNA damage of pesticide factory workers. Occup. Environ. Med., 61: 999-1005.
Bretveld, R.W., C.M.G. Thomas, P.T.J. Scheepers, G.A. Zielhuis and N. Roeleveld, 2006. Pesticide exposure: The hormonal function of the female reproductive system disrupted?. Reprod. Biol. Endocrinol., Vol. 4. 10.1186/1477-7827-4-30
Farr, S.L., G.S. Cooper, J. Cai, D.A. Savitz and D.P. Sandler, 2004. Pesticide use and menstrual cycle characteristics among premenopausal women in the agricultural health study. Am. J. Epidemiol., 160: 1194-1204.
Figa-Talamanca, I., 2006. Occupational risk factors and reproductive health of women. Occup. Med., 56: 521-531.
Figa-Talamanca, I., M.E. Traina and E. Urbani, 2001. Occupational exposures to metals, solvents and pesticides: Recent evidence on male reproductive effects and biological markers. Occup. Med., 51: 174-188.
CrossRef | Direct Link |
Gilden, R.C., K. Huffling and B. Sattler, 2010. Pesticides and health risks. J. Obstet. Gynecol. Neonatal Nurs., 39: 103-110.
Hanke, W. and J. Jurewicz, 2004. The risk of adverse reproductive and developmental disorders due to occupational pesticide exposure: An overview of current epidemiological evidence. Int. J. Occup. Med. Environ. Health, 17: 223-243.
Iyer, P. and S. Makris, 2010. Developmental and Reproductive Toxicology of Pesticides. In: Haye's Handbook of Pesticide Toxicology, Robert, K. (Ed.). 3rd Edn. Academic Press, New York, USA., pp: 381-440.
Malik, J.K., M. Aggarwal, S. Kalpana and R.C. Gupta, 2011. Chlorinated Hydrocarbons and Pyrethrins/Pyrethroids. In: Reproductive and Developmental Toxicology, Ramesh, C.G. (Ed.). Academic Press, San Diego, pp: 487-501.
Mendola, P., L.C. Messer and K. Rappazzo, 2008. Science linking environmental contaminant exposures with fertility and reproductive health impacts in the adult female. Fertil. Steril., 89: e81-e94.
Mostafalou, S. and M. Abdollahi, 2012. The role of environmental pollution of pesticides in human diabetes. Int. J. Pharmacol., 8: 139-140.
Panuwet, P., W. Siriwong, T. Prapamontol, P.B. Ryan, N. Fiedler, M.G. Robson and D.B. Barr, 2012. Agricultural pesticide management in thailand: Status and population health risk. Environ. Sci. Policy, 17: 72-81.
Perry, M.J., 2008. Effects of environmental and occupational pesticide exposure on human sperm: A systematic review. Hum. Reprod. Update, 14: 233-242.
Rahimi, R. and M. Abdollahi, 2007. A review on the mechanisms involved in hyperglycemia induced by organophosphorus pesticides. Pestic. Biochem. Physiol., 88: 115-121.
CrossRef | Direct Link |
Rita, P., P.P. Reddy and S.V. Reddy, 1987. Monitoring of workers occupationally exposed to pesticides in grape gardens of andhra pradesh. Environ. Res., 44: 1-5.
Roeleveld, N. and R. Bretveld, 2008. The impact of pesticides on male fertility. Curr. Opin. Obstetrics Gynecol., 20: 229-233.
CrossRef | Direct Link |
Rupa, D.S., P.P. Reddy and O.S. Reddi, 1991. Reproductive performance in population exposed to pesticides in cotton fields in india. Environ. Res., 55: 123-128.
Shadnia, S., E. Azizi, R. Hosseini, S. Khoei and S. Fouladdel et al., 2005. Evaluation of oxidative stress and genotoxicity in organophosphorus insecticide formulators. Hum. Exp. Toxicol., 24: 439-445.
Snijder, C.A., E. Te Velde, N. Roeleveld and A. Burdorf, 2012. Occupational exposure to chemical substances and time to pregnancy: A systematic review. Hum. Reprod., 18: 284-300.
CrossRef | Direct Link |
Tariq, M.I., S. Afzal, I. Hussain and N. Sultana, 2007. Pesticides exposure in Pakistan: A review. Environ. Int., 33: 1107-1122.
Whorton, M., R.M. Krauss, S. Marshall and T.H. Milby, 1977. Infertility in Male pesticide workers. Lancet, 80: 1259-1261.
CrossRef | PubMed |
Wilson, C. and C. Tisdell, 2001. Why farmers continue to use pesticides despite environmental, health and sustainability costs. Ecol. Econ., 39: 449-462.