This test is most useful if any of these apply to you.
If you live with a smoker, work near industrial fumes, or wonder whether secondhand smoke at restaurants and bars is reaching your bloodstream, this is the marker that answers the question. It tracks acrylonitrile, a chemical your body breaks down within hours of exposure, and shows up in urine even when you don't smoke yourself.
Higher levels have been tied to oxidative damage, inflammation, and a higher likelihood of cardiovascular and metabolic conditions in large population studies. The number is more than a curiosity, it is a window into a class of exposures that standard labs do not measure.
CYMA (N-acetyl-S-(2-cyanoethyl)-L-cysteine, also called 2CYEMA or CEMA) is what your body produces when it detoxifies acrylonitrile. Acrylonitrile is a volatile organic compound, meaning a chemical that evaporates easily into the air you breathe. It is most commonly inhaled from tobacco smoke, including secondhand smoke, and from certain plastics and industrial settings.
Your liver attaches a small protective molecule (called cysteine) to acrylonitrile to neutralize it, and the resulting CYMA gets cleared into your urine. The amount in your urine reflects how much acrylonitrile you have processed in roughly the last day. This is a Tier 3 research marker, meaning it is well-validated as an exposure biomarker in large population studies but does not yet have standardized clinical cutpoints for individual decision-making.
An NHANES analysis of 5,211 U.S. adults found that people with higher urinary CYMA were about 1.8 times as likely to have had a heart attack, after adjusting for other risk factors (odds ratio 1.80, 95% CI 1.14 to 2.83). A separate NHANES analysis of 6,814 adults linked higher CYMA to overall cardiovascular disease risk, alongside other volatile organic compound metabolites.
Higher CYMA has also been associated with higher odds of high blood pressure in a study of 4,156 adults. These are observational, cross-sectional findings, so they show association rather than proof that CYMA itself causes heart disease. They suggest that the exposure CYMA reflects, mostly tobacco smoke and related toxins, is part of a broader pattern of cardiovascular harm.
In a study of 2,531 adults, CYMA was identified as one of the key urinary metabolites associated with metabolic syndrome. Mixture-modeling approaches found that combined exposure to volatile organic compound metabolites, with CYMA among the strongest contributors, tracked with higher metabolic syndrome risk.
A separate analysis of 1,410 U.S. adults found that volatile organic compound exposure, including CYMA, was positively linked with serum lipids, particularly higher triglycerides. The signal points to a connection between this class of inhaled toxins and the metabolic machinery that controls fat in your blood.
In a study of 853 Taiwanese adolescents and young adults, a 10% higher urinary CYMA level was associated with a meaningful rise in 8-hydroxydeoxyguanosine (a marker of oxidative damage to your DNA), with a regression coefficient of 0.325 (p = 0.002). This held up across both genders, in adolescents specifically, in those with higher insulin resistance, and in people exposed to environmental tobacco smoke.
An analysis of 7,007 NHANES participants found that volatile organic compound metabolites, including CYMA, were tied to higher systemic inflammation indices, with smokers identified as the most vulnerable group. Together, these findings suggest CYMA tracks both the chemical hit your DNA is taking and the inflammatory response that follows.
The clearest, most established use of CYMA is as a marker of acrylonitrile exposure from tobacco smoke. NHANES data from 8,057 participants showed that exclusive cigarette smokers had a median urinary CYMA of 145 µg/g creatinine, compared to just 1.38 µg/g in non-users, a more than 100-fold difference. Even people exposed only to secondhand smoke had 36% higher CYMA than fully unexposed individuals after adjustment.
In children, higher CYMA-based exposure profiles were associated with greater healthcare use and more hospitalizations in a study of 2,838 U.S. children. If you live with a smoker, work in hospitality, or spend time in environments where smoking happens, this number can quantify exposure that nicotine testing alone may underestimate.
There are no standardized clinical reference ranges for CYMA. The values below come from a population study of Taiwanese adolescents and young adults (n = 853) and from NHANES biomonitoring data, measured in urine and reported per gram of creatinine. They are illustrative orientation, not clinical targets, and your lab may report different numbers.
| Group | Typical Urinary CYMA | What It Suggests |
|---|---|---|
| Non-tobacco users (NHANES) | Around 1.38 µg/g creatinine (median) | Background exposure from food, plastics, or trace environmental sources |
| Adolescents and young adults (Taiwan) | Around 4.67 µg/L (geometric mean) | Mix of background and low-level secondhand exposure |
| Exclusive cigarette smokers (NHANES) | Around 145 µg/g creatinine (median) | High active acrylonitrile exposure from tobacco smoke |
Sources: De Jesús et al., NHANES 2011-2016; Lin et al., 2018. Compare your results within the same lab over time for the most meaningful trend, since assays and units differ between providers.
A single CYMA reading reflects exposure in roughly the last 24 hours. That short window makes it powerful for verifying whether a specific intervention (quitting smoking, moving away from a smoker, leaving an industrial workplace) actually reduced what is reaching your body, but it also means a single number can be misleading on a one-off day.
Get a baseline. If you are making changes to reduce exposure, retest in 4 to 8 weeks to confirm the new pattern is real. If you are tracking long-term exposure, retest at least annually, or every 3 to 6 months if you live with a smoker or work in an industrial setting where exposure can fluctuate.
If your CYMA is high and you do not smoke, the first step is to identify the exposure source. Look at your home (a smoking partner or roommate), your workplace, your commute (heavy traffic, certain plastics manufacturing), and your social environments. Pair the result with cotinine (a nicotine metabolite that confirms tobacco exposure specifically) and a broader volatile organic compound panel to map the full pattern of exposure.
If your CYMA is elevated alongside markers of oxidative damage (like 8-OHdG) or inflammation (like high-sensitivity C-reactive protein, a blood test for body-wide inflammation), that combination suggests the exposure is producing real biological effects, not just sitting in your urine. That pattern is worth raising with a primary care physician or, if cardiovascular markers are also affected, a cardiologist or preventive medicine specialist.
A few factors can shift a single CYMA measurement without telling you anything meaningful about your long-term exposure:
CYMA is not a diagnostic test for any specific disease. It does not have published sensitivity or specificity numbers for heart attack, hypertension, or metabolic syndrome. It is an exposure biomarker that, in large population studies, tracks alongside higher disease risk. Used as one input in a broader panel, with cotinine, other volatile organic compound metabolites, oxidative stress markers, and inflammatory markers, it gives you a more complete map of how environmental exposures may be affecting your body.
Evidence-backed interventions that affect your NACE level
N-Acetyl (2-Cyanoethyl) Cysteine is best interpreted alongside these tests.