Tobacco, Dust, and Asbestos Exposure at Work Raises Risk for IPF, Australian Study Finds

Tobacco, Dust, and Asbestos Exposure at Work Raises Risk for IPF, Australian Study Finds
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Exposure to secondhand smoke, dust, or asbestos in the workplace is linked to a significantly higher risk of developing idiopathic pulmonary fibrosis (IPF), according to findings of an Australian study.

These results suggest that “the burden of IPF could be reduced by intensified tobacco control, occupational dust control measures and elimination of asbestos at work,” its researchers wrote.

The study “Occupational and environmental risk factors for idiopathic pulmonary fibrosis in Australia: case-control study” was published in the journal Thorax.

Although current antifibrotic therapies are extending IPF patients’ lives slowing disease progression, they have no curative power.

Risk factors underlying IPF are still poorly understood, although their identification is key to reducing risk, especially occupational and environmental risk factors. Their better understanding could also aid the development of preventive strategies, including early diagnosis and screening for at-risk populations.

A group of researchers from across Australia assessed the contribution of potential occupational and environmental risk factors for IPF development in that country.

The team recruited 503 patients with IPF — 346 men and 147 women, mean age of 71.1 — from the Australian IPF registry.

A total of 902 age and sex-matched healthy controls — 625 men and 277 women, mean age of 70.8 — were also recruited.

The impact of environmental factors, including smoking, either tobacco or marijuana; self-assessed exposures, including asbestos, silica, gases/fumes, chemicals, or a dusty environment; a family history of PF or autoimmune disease; and home exposures such as water leaks/mold, farm animals, etc., were assessed.

Results showed that smoking tobacco (ever) was significantly associated with a 2.2 times increased risk of IPF. Current tobacco smoking, however, was linked with a threefold risk reduction. Researchers observed no association between secondhand smoke or pipe smoking outside the workplace and IPF.

After adjusting for age, sex and tobacco smoking (be it never, past, or current), results showed that marijuana smoking reduced the risk of IPF by half.

Keeping birds, exposure to standing water, and potting mix, soil, or compost was also associated with a lower IPF risk.

A family history of pulmonary fibrosis increased the likelihood of IPF by 12.6 times; a family history of autoimmune diseases had no link to IPF risk.

Among occupational exposures, asbestos was directly associated to a 1.4 times greater risk of IPF, while self-reported silica exposure was tied with a risk reduction. Exposure to gases, fumes, chemicals, or dust in the workplace did not seem to associate with IPF.

Exposure to secondhand smoke at work increased by two times the risk for IPF, and ‘respirable dust’ by 1.4 times.

Researchers found that IPF patients had a slight higher mean exposure to asbestos (0.23 fiber.years/milliliter, mL) compared to controls (0.22 fibre.years/mL). Moreover, among IPF cases a proportional increase of disease risk was seen with higher asbestos exposures.

Overall “occupational exposures to secondhand smoke, respirable dust and asbestos were independently associated with increased risk of IPF,” the researchers wrote.

They estimated that 11.6% of IPF risk could be attributed to secondhand smoke in the workplace, 7.6% to respirable dust, and 0.8% to asbestos.

“This finding that such a high proportion of IPF cases are associated with occupational exposures is also extremely important in understanding this otherwise ‘idiopathic’ [unknown cause] disease,” the researchers wrote.

“We conclude that 20% of IPF cases could potentially be prevented by tighter control of workplace smoking, dust suppression, and elimination or substitution of asbestos, together with personal protective equipment, when exposure is unavoidable,” they added.

Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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Patrícia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.
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Patricia holds a Ph.D. in Cell Biology from University Nova de Lisboa, and has served as an author on several research projects and fellowships, as well as major grant applications for European Agencies. She has also served as a PhD student research assistant at the Department of Microbiology & Immunology, Columbia University, New York.
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