chlorine-dermal-absorption-shower

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Chlorine dermal absorption shower searches usually ask one question: does chlorine in shower water pass through the skin? The two sources used here do not measure chlorine itself. They measure disinfection byproducts that form when chlorine reacts with organic matter, and one of them measures how those byproducts cross skin in a laboratory model. That skin data is the most direct evidence in either source. It comes from frozen human cadaver skin in diffusion cells, so it describes what happens to a piece of skin under lab conditions, not what happens to a person who is showering.

Quick answer

• Neither source measured chlorine crossing skin. The skin measurements cover five haloacetonitriles and chloral hydrate, which are byproducts of chlorine reactions.
• In the 2011 lab study, dermatomed skin let the haloacetonitriles through with permeability coefficients from 0.099 to 0.167 cm/hr, while chloral hydrate was 0.0039 cm/hr.
• For bathing, the model in the same paper gives a dermal dose of 0.39 to 0.747 times the ingestion dose for the haloacetonitriles. The model assumed unfiltered water and full gut absorption, so the ratio is an assumption-driven estimate.
• The 2006 breath study of seven people suggests the skin route matters more in a bath than in a shower. It did not measure skin uptake directly, so that is an inference.

What dermal absorption means in these sources

Dermal absorption is the amount of a compound that passes through skin into the body. The Journal of Applied Toxicology paper measures it with a permeability coefficient, written Kp, which it defines as “The skin’s permeability was measured in vitro as the permeability coefficient (Kp) using Fick’s law assuming steady-state conditions.” A higher Kp means a compound crosses skin faster under the same conditions. The paper also notes that the Kp “remains independent of concentration and time and can be applied to many exposure conditions,” which is why it uses Kp to estimate doses at other concentrations.

Two other terms appear in the tables. Lag time is the delay before a compound begins to move through the skin at a steady rate. Steady state is the period after that delay when the flux stays roughly constant. The paper reports that “All compounds measured reached steady-state for the dermatomed skin within an hour,” so the Kp values were calculated from data between 1 and 12 hours.

The paper’s stated reason for the work is a gap in the literature. Its abstract says that “dermal uptake of many DBPs has not been characterized,” and its introduction adds that “Potential dermal exposures to HANs and CH have not been reported.” The study was written to fill that gap for these compounds.

How the skin measurements were made

The experiments used full-thickness and dermatomed torso skin from human cadavers. Dermatomed skin had the dermis removed, leaving the epidermis, cut to a thickness between 0.25 and 0.28 mm. Each piece was placed between two chambers in a side-by-side diffusion cell, held at 37 °C, and stirred. The receiving chamber held a phosphate buffered saline solution that the paper says “was selected to have the same ionic strength and pH value present in blood.” The donor chamber held the test water with the compound at 0.8 g/L for the haloacetonitriles and chloral hydrate.

The paper reports that “Six 12-hr steady-state experiments (3 dermatomed and 3 whole skin samples)” were run. Each skin section was first checked with tritiated water, and sections that let too much of it through were not used. Samples from both chambers were extracted and analyzed with US EPA Method 551.1 by gas chromatography and an electron capture detector. The paper assumes the passage of the compounds was passive. In its words, “It was assumed that any solutes that passed through the skin did so by passive diffusion.”

The paper does not state how many donors the skin came from. Its experiments were six runs in total, three per skin type, so the numbers come from a small set of samples.

The permeation numbers

The table below uses the values from the paper’s Table 4. Kp values are in cm/hr, and lag times are in minutes. Values are means with standard errors where the paper gives them.

Compound	Dermatomed Kp	Whole-skin Kp	Dermatomed lag (min)	Whole-skin lag (min)
Chloroacetonitrile (CAN)	0.0990 ± 0.00840	0.0440 ± 0.000970	6.14 ± 0.500	90.0 ± 18.6
Dichloroacetonitrile (DCAN)	0.146 ± 0.00780	0.0400 ± 0.00190	6.15 ± 0.470	113 ± 25
Trichloroacetonitrile (TCAN)	0.039 to 0.14 (range only)	0.0011 to 0.0072 (range only)	not reported	not reported
Bromochloroacetonitrile (BCAN)	0.155 ± 0.0100	0.0440 ± 0.00370	6.43 ± 0.370	129 ± 30.6
Dibromoacetonitrile (DBAN)	0.167 ± 0.0130	0.0480 ± 0.00440	6.84 ± 0.450	157 ± 43
Chloral hydrate (CH)	0.00390 ± 0.000470	0.00170 ± 0.0000960	not different from zero	208 ± 52

The paper draws three points from these numbers. First, the haloacetonitriles crossed skin much faster than chloral hydrate. The paper states that “The Kps of the HANs were also approximately 30 times that of CH.” Second, the abstract says that “dibromoacetonitrile had the highest permeability while chloroacetonitrile had the lowest permeability,” and the authors report “a direct relationship” between Kp and the octanol/water partition coefficient. The TCAN range in the same table reaches 0.039 cm/hr, below the chloroacetonitrile value, and the paper does not reconcile the two. Third, the whole-skin results were lower. The paper states that “The permeation rate of whole skin is much lower than dermatomed skin.”

The authors give a reason for preferring dermatomed skin for dose estimates. They write that “Thus, using dermatomed skin, where the dermis layer was cut away, provides a better estimate of the dermal absorption in viable skin than using whole skin,” since “in vivo compounds do not need to transverse the dermis to enter the bloodstream.” This is the authors’ argument, not a direct measurement in people.

TCAN is the exception. The paper could only give a range, because its donor concentration fell during the experiment. The authors report losses of 45 to 82 percent and say the fall “is likely due to a degradation of TCAN over time.” For that reason TCAN was excluded from the dose model.

From skin flux to a dose estimate

The paper then turns the Kp values into doses. It states that “The monthly dermal and ingestion doses of HANs and CH of an average American population were estimated using Monte Carlo simulations.” Monte Carlo simulation runs the same calculation many times with randomly selected inputs, so the output is a spread of doses rather than one number. The inputs included body weight, skin surface area, drinking-water intake, bath and pool durations, and water concentrations. The paper used population distributions from an EPA handbook for these inputs, not measured exposures in any home.

The model uses two equations, one for short exposures and one for longer ones, depending on how the exposure time compares with the lag time. Its sensitivity analysis ranked the inputs. The paper states that “For bathing, the key variables were duration of bath and drinking water concentration.” The model’s inputs include shower durations, but the sensitivity result for bathing points to bath length as the main driver, so the bath numbers are the ones most sensitive to that input.

The main output for bathing is a ratio. The paper reports that “The dermal doses are 0.39 to 0.747 times the monthly ingestion doses for the HANs and 0.0160 to 0.0195 times the ingestion dose for CH.” The authors describe this as “a significant fraction of the ingestion doses for the HANs.” For chloral hydrate the dermal share is small, because its Kp is low, even though its drinking-water concentration in the model is higher than that of the haloacetonitriles.

The ingestion comparison has its own assumptions. The paper assumes that gut absorption is complete, stating the efficiency was “assumed to be 100 % to represent a maximal possible dose.” It also assumes that “all of the consumed drinking water was unfiltered tap water to provide an estimate of the maximum ingestion dose.” The skin comparison therefore sits against a high-end ingestion estimate, which is worth remembering before reading the ratio as a head-to-head comparison.

The model separates people by size. The paper states that “The dermal bath and pool water exposures for the children were higher than that of the adults on a per weight basis,” and explains that “This is due to children having a higher surface area per kilogram body mass than adults.” This is a conclusion from the model’s inputs, not a measured difference in children.

Pool water and the swimming result

The paper also estimates pool exposure, but with less data. It states that “Data on pool water concentration was available for only DCAN, DBAN and CH.” For the two compounds with pool data, the paper reports that “The DCAN and DBAN mean pool derived dermal doses are 0.304 to 2.25 times the monthly ingestion doses.” For chloral hydrate, the pool dermal dose was lower, at 0.192 to 0.245 times the ingestion dose, which the paper explains by its low Kp.

The swimming result is the most striking figure in the paper, but it rests on the thinnest data. The authors write that “the dermal dose during swimming is an important contributor to the total dose of these DBPs.” They also note that “It is likely that pool water concentration was not included since few concentrations were available in pool water,” so the sensitivity analysis could not fully test the pool inputs. None of this speaks to showering in a home with a standard shower head.

What the breath study adds

The other source, Gordon and colleagues in Environmental Health Perspectives, did not measure skin uptake. It measured chloroform and bromodichloromethane in indoor air, in exhaled breath and in blood during showers and baths in two homes. The paper’s introduction reads that “Inhalation and dermal contact resulting from showering and bathing have been shown to be significant routes of exposure to THMs,” which is background from earlier studies rather than a result of this one.

The breath results show that bath air levels were lower but breath levels were similar to shower breath levels. The paper’s ratio of breath to air was “0.37 vs. 0.08 for CHCl 3” for bathing and showering. That pattern led the authors to conclude that “the dermal route is the more important exposure pathway (vs. inhalation) in the bath than in the shower.” They support this with a second comparison: “Further confirmation of the importance of the dermal route is provided by a comparison of the effect of secondary shower exposure on the measured air and breath concentrations.”

That is an inference from air and breath data. The study did not separate skin uptake from breathing, and it did not measure any skin compartment. The two sources also do not overlap on compounds: the breath study measured trihalomethanes, and the skin study measured haloacetonitriles and chloral hydrate. A reader cannot take the breath result and apply it to the skin numbers without an extra assumption, and the sources do not supply one.

What the sources do not say

• Chlorine itself. Neither source measured free chlorine crossing skin, and neither reports a chlorine number for skin.
• Skin damage or hair damage. Neither source says that chlorine, or any byproduct, damages skin or hair. This guide makes no such claim.
• Hydration. The paper concedes that “the Kp values calculated using the hydrated skin are applicable to exposures encountered during showering, bathing and swimming when the skin may not become fully hydrated.” Real skin in a shower may absorb differently from fully hydrated lab skin.
• Contact time. The dose model assumed the lab Kp values “are applicable to shorter water contact times.” The paper does not measure contact times for an actual shower.
• Filters. The model assumed unfiltered water. Neither source evaluated a filter or a shower head.
• Concentrations. The lab donor concentration was 0.8 g/L. The same paper says haloacetonitriles typically reach levels as high as 24 µg/L in drinking water, a figure it attributes to earlier work. The lab result describes a much stronger solution than typical shower water.
• Health outcomes. The paper calls dermal exposure “a significant route of exposure” for these compounds, and it notes that “dermal contact is a potentially significant route of exposure due to their high Kp values.” It does not measure any health effect from that exposure.

How we chose

This article uses the skin-permeation paper as the main source for permeation values and dose estimates. The breath paper is used for the activity-level context and for the one inference about bath versus shower. Both were read from saved full-text copies in the site research folder, checked on 2026-10-28, and every direct quotation was checked against those saved texts. A third saved file in the folder was not used, because the brief limits this guide to these two sources. Numbers come from the papers’ tables, and the arithmetic in this article is limited to reading those tables.

What we could not verify

• How many people the cadaver skin came from. The paper does not say.
• Whether permeation through living, hydrated skin during a real shower matches the lab Kp values. The paper says this is uncertain.
• The exposure inputs for the dose model. The paper cites earlier concentration surveys and an EPA handbook for these, and those sources were not opened for this guide.
• The earlier estimates quoted inside the paper. Brown and colleagues (1984) estimated that “an average of 64% of a total dose to lipophilic compounds in drinking water from showering is accounted for by dermal exposure,” and a 1990 estimate put the daily dermal chloroform dose from showering near the ingestion dose from two liters of tap water. Both are cited inside the paper and were not checked against their own papers.
• Whether any of these values apply to a shower head, a filter, or a particular city’s water today.

FAQ

Does chlorine pass through the skin during a shower?

Neither source measured that. The skin study measured haloacetonitriles and chloral hydrate, which are byproducts formed when chlorine reacts with organic matter in water. The question about chlorine itself is not answered by these sources.

Which of the measured compounds crossed skin fastest?

In the lab study, dibromoacetonitrile had the highest dermatomed Kp, at 0.167 cm/hr. The abstract calls chloroacetonitrile the least permeable, at 0.0990 cm/hr as a single value, but the TCAN range reaches lower numbers, so the ranking at the bottom is not clean. Chloral hydrate was much slower, at 0.0039 cm/hr. These are lab values from frozen cadaver skin.

Is skin absorption more important than drinking water?

For the haloacetonitriles in the modeled bathing scenario, the dermal dose was 0.39 to 0.747 times the ingestion dose. For chloral hydrate it was much smaller. The ingestion side assumed full absorption and unfiltered water, and the model’s inputs are population estimates. The ratio is not a measured comparison for any one person.

Does a shower filter reduce skin absorption?

The sources do not say. The model assumed unfiltered tap water, and neither source evaluated a filter or a shower head.

Does chlorine damage skin or hair?

Neither source says so, and this guide does not claim it. The sources cover absorption of byproducts through lab skin and exposure in a small breath study. They do not cover skin or hair condition.

When should I see a doctor?

If you have skin irritation, itching, or a rash after showering, talk to a doctor or a dermatologist. If you have breathing symptoms, talk to a doctor. This guide does not give medical advice and cannot assess an individual’s risk.

Bottom line

The skin data in the Journal of Applied Toxicology paper show that haloacetonitriles cross human skin in a lab model, and that chloral hydrate crosses much more slowly. The paper’s dose estimates depend on assumptions about hydration, contact time, unfiltered water and full gut absorption. The breath study points toward skin as a route in the bath, but it is small and does not measure skin uptake. Neither source measures chlorine itself, so the chlorine question stays open.

Sources

• Trabaris M, Laskin JD, Weisel CP. Percutaneous Absorption of Haloacetonitriles and Chloral Hydrate and Simulated Human Exposures. J Appl Toxicol. 2011;32(6):387-394. doi:10.1002/jat.1657. https://pmc.ncbi.nlm.nih.gov/articles/PMC3199364/ (opened 2026-10-28)
• Gordon SM, Brinkman MC, Ashley DL, et al. Changes in Breath Trihalomethane Levels Resulting from Household Water-Use Activities. Environ Health Perspect. 2006;114(4):514-521. https://pmc.ncbi.nlm.nih.gov/articles/PMC1440773/ (opened 2026-10-28)