Plastics and cardiovascular deaths: is it time for global plastics regulations?

Plastic takeaway food containers containing rice
Phthalates make plastics more flexible. Credit: DigiPub/Getty Images

The issue of how much chemicals used in plastics contribute to heart disease has risen again after a new research paper claimed that a type of phthalate is associated with hundreds of thousands of deaths.

The latest study estimates that a chemical additive in plastic contributed to more than 356,000 cardiovascular disease deaths among men and women aged 55-64 in 2018 across the globe.

This would account for more than 13% of all cardiovascular disease deaths within the age group.

The authors from New York University (NYU) claim that their findings underscore “the need for urgent global policy interventions aimed at reducing exposure to phthalates” and calls for “immediate regulatory action to mitigate these risks.”

But not everyone finds the paper, which was published in the journal eBioMedicine, alarming.

At issue is di-2-ethylhexyl phthalate (DEHP) a “plasticiser” used in food packaging and medical equipment. It makes them softer and more flexible.

“As with other plasticisers, this phthalate is loosely held in the plastic and known to migrate out of the plastic throughout its life cycle,” Dr Christos Symeonides, a paediatrician and researcher in Plastics and Human Health at the Minderoo Foundation, told Cosmos. He was not involved in the research.

DEHP is a “a known endocrine-disrupting chemical with consistent findings of adverse human health impacts”, says Symeonides, who co-authored a recently published formal Umbrella Review on the health effects of plastics.

“Despite health concerns, global research measuring the metabolites of this chemical in urine shows that we are essentially all exposed to this chemical each day to differing degrees.

“The paper…extends our understanding of how associations that have been seen with disease in individual research studies translates to typical levels of exposure on a global scale.”

The NYU team brought together its previous work – a review of publicly available global biomonitoring data on the breakdown products of DEHP in urine, and research estimating the link between DEHP and heart disease in the US – to estimate DEHP exposure and what role this may have had in the deaths of people aged 55-64 in 200 countries and territories.

“The methodology of this analysis … is similar to those we have used ourselves in a paper that colleagues and I independently published last year,” says

Symeonides, who adds their recent study showed “very similar findings in relation to the likely global health impacts that can be attributed to DEHP exposure in this 55–65-year-old age range, although we were looking at all causes of death.”

They estimated that DEHP exposures were linked to approximately 164,000 deaths among 55-to-64-year-olds.

“Our numbers are a little lower because we restricted our findings to 38 countries for which we could find suitable exposure data.

“The exposure data used in the New York University [study] takes an additional step to model exposure in all countries, based on regional data.”

The findings are controversial.

Dr Oliver Jones, a professor of chemistry at RMIT University who was not involved in the research, says that “the results need to be interpreted with care”.

“I think claiming that we need ‘immediate regulatory action’ as a result of this paper is a large overstretch,” Jones told Cosmos.

“At best, it only tells you there may be an association between DEHP exposure and health outcomes. The problem is that association is not causation, and other factors are likely causing the association.”

A major use of DEHP is in medical devices such as blood bags, tubing and catheters, Jones says.

“People with existing health conditions severe enough to undergo such medical treatments are thus more likely to be exposed to DEHP as a result of their treatment, meaning they would have higher concentrations of DEHP metabolites in their blood or urine than most of the population,” says Jones.

“This would mean the DEHP was a result of treatment for existing disease not the cause of said disease. 

“The death rate of people with pre-existing conditions (e.g. heart disease) severe enough to require the use of medical devices or medications is likely to be higher than the general population average anyway and has nothing to do with DEHP. This is unlikely to be improved by reducing or banning non-medical DEHP to minimise exposure.”

Another common use of DEHP is in food containers and packaging, he adds.

“So if you eat a lot of this type of (junk) food, you will have a higher exposure to DEHP than people who don’t,” he says.

“However, eating a lot of this kind of food itself may lead to various adverse health outcomes, such as heart problems. The DEHP exposure is again incidental to eating a lot of junk food, but it is the junk food that causes health issues, not the DEHP.”

As the global study used aggregate data at the country level, it wasn’t possible to incorporate information on these individual-level confounders.

“Another issue is that the authors are using something called attributable mortality in this paper,” says Jones.

“This means they are trying to estimate the number of deaths or cases of disease (in this case, cardiovascular disease and associated deaths) that would not have happened had a particular factor (in this case, DEHP) exposure not occurred.

“However, cardiovascular disease has many causes, and the idea that one can use attributable mortality to work out what proportion of total deaths from cardiovascular disease were due to DEHP and which were not, when multiple factors are involved in the disease and when there is no group when DEHP exposure was actually reduced in the data … is problematic.”

Symeonides says the limitations of the paper are well described in its discussion.

“Heart disease is a complex multifactorial disease and there are limitations in extrapolating data on contribution of DEHP, or any other single factor from a single study in a single country, across to other populations where the mixture of other contributing factors may be very different (rates of smoking, obesity, etc),” says Symeonides.

“In another population the contribution of a given increase in exposure to DEHP may be greater or smaller because of the other factors in play, but the epidemiological data that we have available is often limited and these assumptions become necessary to start estimating effects outside of the small number of countries where epidemiological research is being done.”

Much of the peer-reviewed research is concentrated in higher resource countries.

“Taken together with an extensive literature on human health impacts, not just of phthalates, but of other chemicals such as bisphenol A (BPA) and polybrominated diphenyl ethers (PBDEs) released from plastics and included in our Umbrella Review, these new findings add further support for the need for global plastics regulations,” Symeonides concludes.

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