N-Acetyl (2-Cyanoethyl) Cysteine

Most people never find out how much tobacco smoke their body is actually taking in, whether from their own cigarettes or someone else's. This urine test answers that question directly by measuring a chemical fingerprint of one specific smoke toxicant. It catches exposure that a standard checkup would completely miss.

The value here is not diagnosing a disease. It is knowing, in real numbers, whether smoke exposure is reaching your body and whether the steps you take to reduce it are working.

What This Marker Actually Measures

This test measures CYMA (N-acetyl-S-(2-cyanoethyl)-L-cysteine), a waste product your body creates when it clears acrylonitrile, a toxic chemical produced when tobacco and other organic material burn and also used in making plastics and synthetic fibers. Your body attaches the acrylonitrile to a small protective molecule and eventually sends it out in urine as this compound. A higher urine level means more acrylonitrile has recently entered your body.

For most people who are not exposed at work, acrylonitrile comes almost entirely from combustion, so this marker sits close to zero in people who avoid smoke. That makes it a clean signal of real exposure rather than background noise. It is used in research and public health as a way to track acrylonitrile exposure, not as a stand-alone diagnostic test for any illness.

Cigarette Smoke Is the Dominant Source

Burning tobacco is by far the biggest source of this marker. In a large US national health survey, people who smoked cigarettes had levels roughly 100 times higher than non-users (a median of 145 versus 1.38 micrograms per gram of creatinine). The number climbed steadily with each additional cigarette per day, and even light smoking of one to ten cigarettes daily was tied to levels about 68 times higher than in non-users.

The signal is sharp: in one study this marker separated cigarette smokers from nonsmokers with more than 99% accuracy, while a large national survey analysis found somewhat lower but still strong accuracy. It stays very low in people who use non-combusted products such as e-cigarettes or smokeless tobacco, because those do not involve burning. That is what makes it useful for confirming whether combusted smoke is truly reaching your body.

Secondhand and Other Burning Smoke

You do not have to smoke to carry this exposure. In the same national survey, people with signs of secondhand smoke exposure had about 36% higher levels than unexposed people, despite reporting no cigarettes of their own. Living or spending time around smokers leaves a measurable mark.

Other burning sources contribute too. Cannabis smoke raises this marker, though less than cigarettes do. Because burning organic material of any kind can release acrylonitrile, passive smoke from barbecues and campfires may also add to it, though this specific source is less firmly established.

Oxidative Damage to DNA

Higher exposure tracks with more damage to DNA from unstable oxygen molecules, a process called oxidative stress. In a study of 853 adolescents and young adults, people with higher levels of this acrylonitrile marker also had more of a urine marker of oxidative DNA damage (called 8-OHdG, short for 8-hydroxydeoxyguanosine).

This link held across sexes, in adolescents, and in those exposed to environmental tobacco smoke. In that particular study, the marker was not tied to traditional heart disease risk factors, which points to oxidative damage as an early, exposure-driven effect rather than a downstream one.

Lung Function

Higher levels of this marker have been linked to weaker breathing capacity. In an urban cohort of about 3,500 adults, people with higher urinary acrylonitrile metabolite had lower measures of how much air they could move (including forced vital capacity and one-second breathing volume), and their lung function declined faster year over year.

Markers of inflammation and oxidative damage explained a portion of that effect, roughly 6% to 36%. People with healthier overall lifestyles showed a smaller decline for the same exposure, which suggests the harm is not fixed.

Cardiovascular and Metabolic Signals

Several large analyses from a US national health survey have connected higher levels of this marker to cardiometabolic conditions: prior heart attack, high blood pressure, metabolic syndrome, higher triglycerides, and higher systemic inflammation. These are cross-sectional snapshots, meaning they measure exposure and disease at the same moment rather than following people forward.

Because this marker rises with smoking, much of the association likely reflects the well-established harms of smoke itself rather than proof that acrylonitrile alone causes these conditions. Read it as a red flag for exposure and its known consequences, not as a diagnosis.

Sources: Kong and Qiu 2025 (heart attack); Lin et al 2018 (DNA damage); Wan et al 2025 (lung function).

What this means for you: a high result is a reason to find and remove the smoke source, not to assume you already have heart or lung disease. The most useful move is to lower the exposure and then confirm the number drops.

Recent Exposure, Not Lifetime Burden

This is a short-term marker. Smoke-related urine compounds like this one clear quickly, within roughly a day or two of exposure, so a single sample mostly reflects your most recent exposure. If you want a marker of long-term, cumulative exposure, blood-based measurements of chemical-protein adducts, which reflect a longer window, serve that role instead.

In people who smoke regularly, levels stay fairly steady over time, with good repeat consistency (a consistency score of about 0.67, where 1.0 would be identical every time). That steadiness comes from a repeated daily habit, not from the chemical lingering in your body for years.

Why One Reading Is Not Enough

Because this marker responds quickly to exposure, its real power is in the trend. A single value tells you about the past day or two, but a series tells you whether your exposure is genuinely falling. That is exactly what you want when quitting, moving away from a smoky household, or switching off combusted products.

A practical rhythm: get a baseline, retest two to four weeks after making a change, then periodically to confirm the number stays down. Since combustion is the near-exclusive source for most people, a drop toward nonsmoker levels is strong evidence that your change is working.

What to Do With an Unexpected Result

If your level is high and you do not smoke, treat it as a prompt to hunt for a combustion source: a household or car smoker, a workplace exposure, smoked cannabis, or frequent grilling. Pairing this test with a urine nicotine marker (cotinine) helps separate nicotine exposure from burning, since vaping and smokeless tobacco raise cotinine but not this marker.

To understand downstream effects, an oxidative DNA damage marker and a general inflammation marker (hs-CRP, high-sensitivity C-reactive protein) add context on whether the exposure is leaving a biological footprint. If the level stays high after you remove the obvious sources, an occupational or environmental review is worth considering.

When a Single Reading Can Mislead

• Timing of exposure: because this marker reflects the last day or two, one smoky evening can raise it briefly even if your usual exposure is low. A single spike is not the same as a chronic pattern.
• Fasting: longer fasting may slightly lower the number, a small artifact rather than a real change in exposure.
• Hydration and kidney function: spot urine is adjusted for concentration using creatinine, so dilution and kidney function can shift the raw value without changing your true exposure.
• Sampling near an event: collecting right after grilling, a campfire, or time in a smoky room captures that moment rather than your typical exposure.