The risk of amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, may be increased with exposure to pesticides, suggests a new study published in JAMA Neurology.
Amyotrophic lateral sclerosis (ALS) is a progressive, neurodegenerative disease that attacks the nerve cells, or neurons, in the brain and spinal cord that are responsible for voluntary muscle control.
Early symptoms of ALS include walking difficulties, muscle weakness, muscle cramps, and slurred speech.
According to the National Institute of Neurological Disorders and Stroke (NINDS), it is estimated that more than 12,000 people in the United States have received an ALS diagnosis.
Around 5-10 percent of ALS cases are inherited, with around a third of such cases resulting from a mutation in a gene called C9orf72.
However, NINDS note that for the remaining 90-95 percent of ALS cases, no clear risk factors for the disease can be identified.
Now, study co-author Dr. Eva L. Feldman, of the University of Michigan, and colleagues suggest that exposure to pesticides – particularly organochlorine pesticides (OCPs), such as dichloro-diphenyl-trichloroethane (DDT), methoxychlor, and benzene hexachloride – may increase a person’s lifetime risk for ALS.
Pesticides are chemicals used to protect crops and livestock from pests – including pathogens, insects, and animals – that might damage or destroy them.
However, the U.S. Environmental Protection Agency (EPA) banned the use of DDT in 1972, after it emerged that the pesticide posed a number of health risks to wildlife and humans.
For their study, Dr. Feldman and colleagues enrolled 156 patients with ALS and 128 controls without the disease.
Full data on occupational and residential exposure to pesticides – including OCPs, polychlorinated biphenyls (PCBs), and brominated flame retardants (BFRs) – and the presence of pollutants in the body were gathered for 101 ALS patients and 110 controls through surveys and blood sampling.
The researchers found that both the presence of pesticides in the blood and residential and occupational pesticide exposure was associated with increased risk of ALS, and this association was particularly strong for exposure to OCPs.
After accounting for possible confounding factors, including participants’ age, sex, education level, smoking status, and information on occupational risk factors, the team found the link between pesticide exposure and increased ALS risk remained.
Commenting on their results, the authors say:
“Our findings identify classes of pollutants that increase the likelihood of ALS and therefore are modifiable disease risk factors.
[…] as environmental factors that affect the susceptibility, triggering, and progression of ALS remain largely unknown, we contend future studies are needed to evaluate longitudinal trends in exposure measurements, assess newer and non-persistent chemicals, consider pathogenic mechanisms, and assess phenotypic variations.”
In an editorial linked to the study, Jacquelyn J. Cragg, of the Harvard T.H. Chan School of Public Health in Boston, MA, and colleagues hail the study as an “important effort in the quest to better understand the role of environmental and occupational exposures in the development of ALS.”
However, they point out that such studies would be more effective if data on pollutant exposure is collected prior to ALS development, though they admit doing so is challenging.
“[…] the relative rarity of ALS makes cohort studies difficult,” they note, “and when they can be done, data are not always available on many exposures of interest.”