Campus & Community

It’s not the sun’s or smoke’s fault, it’s the asphalt

5 min read
Mike McClean has taken a close look at the workplace exposure of asphalt workers. (Staff photo by Stephanie Mitchell)

Most people in America are familiar with the words “black lung disease,” first used in 1942 to describe a painful and often fatal occupational hazard to coal miners who breathe in particulates day after day. Black lung and other perils of coal mining are well known, though the population of miners in the United States is relatively small – only about 208,000.

By contrast, there are approximately 500,000 asphalt workers in the United States today who have significantly increased risk of lung, stomach, bladder, and nonmelanoma skin cancer – yet little is known about this particular occupational hazard, and it was rarely studied until the early 1990s. Mike McClean, Sc.D. ’03, a researcher at the Harvard School of Public Health, is just one of a handful of scientists who are studying asphalt workers to determine whether this increased risk of disease results from workplace exposure.

“Asphalt is used primarily in the roofing and paving industries,” says McClean, who conducted his experiments under the advisement of principal investigator Robert Herrick, a senior lecturer on industrial hygiene in the Department of Environmental Health. “And though it is not currently classified as a carcinogen, it contains a complex mixture of chemicals called polycyclic aromatic hydrocarbons, or PAHs. And many of those are either known or suspected carcinogens.”

When petroleum is broken down into “all the parts that are useful,” such as gasoline and diesel fuel, a thick, dark, PAH-laced liquid remains. This liquid is used as a binding agent with a mineral aggregate – sand, crushed stone, and so forth – to make the gooey sludge we know as asphalt. The asphalt is laid onto roadbeds by a team of four kinds of workers. There’s the paver operator, who drives the large hopper that contains the asphalt; the screedmen, who control the thickness and width of the asphalt patch that’s laid down; the roller operator, who smoothes the hot gunk; and the rakers, or laborers, who use shovels and rakes to get the asphalt into hard-to-reach places – near curbs, for example.

It is known that there’s an increased chance of cancer for asphalt workers overall, but who is most at risk, and why?

To find out, McClean conducted a three-part study. The first part measured inhalation exposure – that is, how much asphalt fume gets into a worker’s lungs – and dermal exposure, or how much asphalt clings to the mens’ skin. For the former, a small air pump attached to the workers’ collars measured the same air they were breathing; for the latter, an adhesive patch was attached to the workers’ wrists. “But only a small portion of the exposure that workers get on site is absorbed and gets inside their body,” says McClean.

To learn how much, he and his colleagues collected preshift, postshift, and bedtime urine samples from the 49 workers they studied over multiple days. They then measured the amount of 1-hydroxypyrene, a biomarker for a principal chemical component of PAHs, excreted in the urine.

“But of everything that’s absorbed into the body,” says McClean, “only a portion results in a biologically effective dose. So the exposure of concern gets smaller and smaller as we move forward in time. For a chemical to be biologically effective it has to reach the target of interest. In this case, because the health effect is cancer, the target of interest is DNA.”

In the final step of his research, McClean used blood samples to measure PAH adducts – that’s short for “addition products” – that were binding to the workers’ DNA. “It’s been shown in previous studies,” McClean notes, “that adduct formation correlates well with cancer risk. So it’s a marker of DNA damage. Sort of a wrench in the works. Ultimately, we wanted to see if inhalation and dermal exposure to PAHs was associated with DNA adduct burden, because if it was, then that would suggest these exposures increase risk of cancer.”

They found that the DNA damage increased during each day of the work week, suggesting that asphalt exposure resulted in increased cancer risk. Also, PAH exposure was greater when workers were exposed to recycled asphalt; though McClean isn’t quite sure why, he suspects it has to do with the higher temperature needed to soften the stuff sufficiently for application.

Exposure varied according to task. Inhalation estimates were consistent with the workers’ proximity to the source of fumes – the paver operators had the highest number of micrograms per cubic meter, and laborers the lowest. Dermal contact was highest for the laborers, and lowest for the roller operators.

Furthermore, urinary tests showed that the amount of PAHs absorbed into the body was more from dermal exposure than from inhalation. In fact, the contribution of dermal exposure was an astonishing eight times higher than that of inhalation.

This is an important finding because, says McClean, “Historically, inhalation exposure received more attention. But it is becoming clear that dermal is more important than was originally thought. So in terms of cancer-prevention strategy, focusing on dermal exposure will be the most effective way to protect workers.” And controlling dermal exposure seems relatively straightforward: cover the skin better by always wearing gloves and long-sleeved shirts, and wash up more frequently. McClean is currently discussing his results and determining recommendations with the asphalt industry.

“Improved hygiene at the site would likely make a big difference,” McClean points out, “but that’s easier said than done. How do you get running water to a highway?”