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Table of Contents
Genetics of ear wax
Summary
Your earwax is either wet, sticky and yellow or brown, or it is dry, crumbly and grayish. Unlike every other human character on these pages, this actually is a simple genetic trait. Whether you have wet or dry earwax is determined by a single gene with two alleles, and the allele for wet earwax is dominant. So if you have wet earwax and both your parents have dry earwax, one or both of your parents probably isn't your biological parent. Maybe you were adopted and they haven't told you, or maybe they used a sperm donor or an egg donor, or maybe there was a mixup at the hospital, or maybe your Mom had an affair. This is one of the reasons I don't recommend that teachers use common human traits to teach genetics.
Are there just two kinds of earwax?
Earwax, also known as "cerumen," is produced by glands that line the ear canal. It gradually moves out of the ear, carrying dead skin cells and other debris. Most people have either wet or dry earwax. Wet earwax is sticky and yellowish brown to dark brown in color, while dry earwax is crumbly (like the crumbs from a pencil eraser) and gray to tan. A small number of people, generally less than 1 percent, have earwax that is intermediate or unclassifiable (Matsunaga 1962, Petrakis et al. 1967; Ing et al. 1973; Petrakis et al. 1990). But unlike several of the traits discussed in these pages (earlobes, widow's peak, PTC tasting), earwax really is a trait with two distinct categories, not a smooth distribution with lots of intermediates.
Most people know what kind of earwax they have (once you tell them there are two different kinds). But when wet earwax makes its way to the outer ear, it can dry out a bit, so that someone with wet earwax might think, "My earwax is kind of dry and a little bit crumbly, do I have wet or dry earwax?" Instead of just asking people if they have wet or dry earwax, rigorous scientific research on the trait requires having a medical professional carefully and safely swab wax from inside the ear canal. The difference is then very obvious.
Family studies
Matsunaga (1962) wrote the first English-language paper on the polymorphism in earwax type, reviewing a large body of Japanese-language literature that dated back to the early 1930s. Data on Japanese families showed the following, where "W" is wet earwax and "D" is dry earwax:
| Parents | W offspring | D offspring |
|---|---|---|
| W×W | 35 | 12 |
| W×D | 205 | 195 |
| D×D | 0 | 634 |
If the allele for dry is recessive, two parents with dry earwax could not have a child with wet earwax, and this is what the data show. In addition, because the allele for wet earwax is rare in this sample, most W parents would be WD heterozygotes. You would then expect about a 3:1 ratio of W to D in offspring of WxW matings, and about a 1:1 ratio of W to D in WxD matings. The data also fit this prediction. These data support the conclusion that earwax is one-locus, two-allele trait, with the W allele being dominant.
Petrakis et al. (1967) performed a similar study in American Indians, with similar results:
| Parents | W offspring | D offspring |
|---|---|---|
| W×W | 32 | 6 |
| W×D | 20 | 9 |
| D×D | 0 | 42 |
and so did Nakajima and Hirano (1969) in Japan:
| Parents | W offspring | D offspring |
|---|---|---|
| W×W | 27 | 3 |
| W×D | 137 | 109 |
| D×D | 0 | 345 |
So unlike nearly other trait I discuss in these pages, earwax really is a simple genetic trait, controlled by one gene with two alleles, with one allele (for wet earwax) completely dominant over the other.
Genome studies
Tomita et al. (2002) used eight Japanese families to determine that the gene for wet/dry earwax is on chromosome 16, near the centromere. Yoshiura et al. (2006) then found the gene responsible: ABCC11 (ATP-binding cassette, subfamily C, member 11). The allele for wet earwax has a G at site 538 of the coding region, which causes a glycine at position 180 in the amino acid sequence; most dry alleles have an A at site 538, coding for arginine. There is another, less common allele, a deletion of 27 nucleotides in exon 29, that also causes dry earwax.
Ile Ala Ser Val Leu Gly Pro Ile Leu Ile Ile Pro
wet earwax ATT GCC AGT GTA CTC GGG CCA ATA TTG ATT ATA CCA
dry earwax ATT GCC AGT GTA CTC AGG CCA ATA TTG ATT ATA CCA
Arg
Bases 523-558 of the coding sequence of ABCC11, along with the amino acid sequence. The DNA polymorphism at site 538 causes the amino acid polymorphism that determines earwax type.
Functional basis for the phenotypes
Toyoda et al. (2009) stained earwax gland cells for the ABCC11 protein and found that cells with the wet earwax genotypes (GG and GA) had much more of the protein, and it was located in granules and vacuoles within the cells, while the dry earwax genotype (AA) had much less ABCC11 protein, and it was spread throughout the inside of the cells. They figured out that this was because substituting an arginine (which is positively charged) for a glycine (which is neutral) caused the protein to be folded incorrectly; the cell recognizes the defective protein and rapidly degrades it. Toyoda et al. (2017) made transgenic mice that expressed the human ABCC11 gene, and found that cells of mice with the human G allele contained the human ABCC11 protein, while mice with the human A allele did not contain the protein. They did not report whether mice with the G allele had wet mouse earwax or stinky little mouse armpits.
Natural selection on earwax alleles
The ABCC11-A allele for dry earwax has frequencies close to 100% in people from northern China and Korea, is intermediate in people from Japan, southern Asia, and American Indians, is uncommon in Europe, and is almost completely absent in Africa (Petrakis et al. 1971, Ibraimov 1991, Yoshiura et al. 2006, Ohashi et al. 2011). There are very few polymorphisms in the human genome that show this much difference in allele frequency between one geographic area and another. Geographic variation can be caused by either natural selection, or random genetic drift, but random drift will affect all genes about the same. So when one gene shows much more geographic variation than most other genes, it is evidence that the geographic variation is caused by natural selection (Lewontin and Krakaur 1974, McDonald 1994), so it seems pretty clear that ABCC11 is affected by natural selection.
Ohashi et al. (2011) used patterns of variation at two nearby microsatellite loci and estimated that the allele for dry earwax originated as a new mutation about 2000 generations ago and has spread due to natural selection, with dry earwax individuals having a relative fitness about 1 percent higher than wet earwax individuals. The ABCC11-G allele for wet earwax is more common in warmer areas in Europe, Asia and the Americas (Ohashi et al. 2011), so one possibility is that something about cooler climates favors the dry earwax allele in cool areas and the wet allele in warm areas. Another possibility is that the ABCC11-A alllele is universally more fit (perhaps because it causes reduced body odor), is spreading outwards from its east Asian origin, and will eventually increase in frequency everywhere (Martin et al. 2010).
Earwax and body odor
You have two kinds of sweat glands: eccrine sweat glands, which are found throughout your skin, and apocrine sweat glands, which are found in your armpits and groin. Eccrine sweat glands produce sweat that is mostly water and salt, and it does not contribute very much to body odor. Apocrine sweat contains proteins and lipids; when bacteria on the skin metabolize apocrine sweat, they produce body odor. The earwax glands (ceruminous glands) are another form of apocrine gland, so genetic variation that affects earwax glands could also affect sweat glands.
In Japan, wet earwax has long been associated with greater body odor (Adachi 1937, Matsunaga 1962). Yoo et al. (2006) found that 860 out of 896 patients who consulted a doctor about axillary osmidrosis (the medical term for stinky armpits) had wet earwax, in a population where wet earwax is uncommon. Nakano et al. (2009) genotyped the polymorphism in the ABCC11 gene in Japanese axillary osmidrosis patients and found the genotypes that cause wet earwax in 78 out of 79, while only 35 percent of the general population had wet earwax genotypes; Inone et al. (2010) and Ren et al. (2016) found similar results. Martin et al. (2010) analyzed sweat from people of different ABCC11 genotypes and found that several compounds that are precursors for body odor are absent or in lower concentrations in sweat from people with the dry earwax genotype.
Rodriguez et al. (2013) genotyped about 6500 white women in England at the ABCC11 polymorphism and asked them about their deodorant use. Of the women with the AA genotype (dry earwax), 17% never used deodorant, while only 4% of the women with the wet earwax genotypes (GG and GA) said that they never used deodorant.
Earwax and breast cancer
Like the earwax glands, the mammary glands are a form of apocrine gland, and the ABCC11 gene is expressed in both. Petrakis (1971) noticed that breast cancer was less common in geographic areas with high frequencies of dry earwax. He found a higher frequency of wet earwax in Japanese-American women with breast cancer than in a control group of Japanese-American women, although the difference was not statistically significant. Ing et al. (1973) surveyed a much larger sample of breast cancer patients and controls in Hong Kong and did not find a significant difference in the frequency of wet earwax.
Ota et al. (2010) compared ABCC11 genotypes in Japanese breast cancer patients and controls and did find a significantly higher frequency of the allele for wet earwax in breast cancer patients; the genotypes for wet earwax were in 25 percent of the cancer patients and 17 percent of the controls. There was no difference in ABCC11 genotype frequency between breast cancer patients and controls in large samples of German (Lang et al. 2011), Australian or Italian (Beesley et al. 2011) women, but fewer than 2 percent of women in those populations have dry earwax.
There is additional evidence that the ABCC11 polymorphism affects the mammary glands. Breast fluids can be collected from some women who are not producing milk, and Petrakis et al. (1981) found that both Asian and Caucasian women with wet earwax were more likely to produce breast fluids. Petrakis et al. (1990) confirmed this pattern, but found that there was a larger difference between wet and dry earwax women for Asian immigrants to the United States than for U.S.-born Asian-Americans, suggesting that the environment also plays a role. Miura et al. (2007) found that women with dry earwax were less likely to produce colostrum (the breast milk produced around childbirth), and those who did produced smaller volumes than women with wet earwax.
Several papers have found that people with different ABCC11 genotypes respond differently to cancer chemotherapy drugs (Uemura et al. 2010, Magdy et al. 2013, Tsuchiya et al. 2015, Uemera et al. 2019, Hlavác et al. 2020).
Should you use earwax to teach genetics?
Unlike most of the human characters that biology teachers use to demonstrate simple genetics principles, whether you have wet or dry earwax really is controlled by one gene with two alleles. And there's a lot of other fascinating information about it: the gene has been identified, the biochemical basis for the variation is fairly well understood, there is evidence for strong natural selection, and there are links to human health (body odor and possibly cancer). The G/A polymorphism in ABCC11 causes a polymorphism in a restriction site for the restriction enzyme DdeI, so a simple PCR+restriction digest reaction can be used as a classroom laboratory exercise to genotype the polymorphism (Hayashida et al. 2010).
There are, however, problems with using earwax type in the traditional classroom exercise, where everyone records their phenotype on a worksheet (a very short worksheet, after you've read all of these pages and crossed off tongue rolling, attached earlobes, and the other popular traits). One is that the allele for dry earwax has a frequency in western European populations of 10 to 20 percent, and it is virtually absent from African populations. Because dry earwax is recessive, this means that a classroom of students of European and African ancestry may show no variation; everyone could have wet earwax, which is a pretty boring result. Classrooms in northern China or Korea, on the other hand, may contain only students with dry earwax, because the allele for dry earwax is at nearly 100 percent in those areas.
In a classroom of students with a mix of ancestries, wet vs. dry earwax could turn out to be a marker of ancestry; most of the students of east Asian ancestry would have dry earwax, and most of the students of European or African ancestry would have wet earwax. Dividing a class into wet and dry earwax, and ending up with all the Black and white students on one side of the room and all the Asian students on the other side, really seems like a bad idea. And once you tell the students that people with wet earwax have more body odor, expect the teasing to get pretty vicious.
A pretty consistent figure around the world is that about 1% of children have "unacknowledged non-parentage," meaning that the child doesn't know that one or both of the people they call Mom and Dad are not their biological parents. If you're a teacher, do you really want your class to be where one of your students finds this out about their family?
I do talk about earwax when I teach genetics to upper-level undergraduates, but I don't ask them what kind of earwax they have. I'm not sure I would mention it if I were teaching middle or high school.
Further research
There's lots of molecular, cellular, physiological, and evolutionary research that should be done on ABCC11, especially since it may provide some insights into cancer, but I can't think of the kind of simple, low-tech projects that could be done as a high school or undergraduate project. High school students have genotyped the ABCC11 polymorphism to determine the allele frequencies in different population samples (Super Science High School Consortium 2009), but since the geographic patterns of allele frequency are already well described, it's not clear what more can be learned from this.
It is well established that people with dry earwax have less body odor, and the allele for dry earwax has increased in frequency in east Asia pretty rapidly (rapid in evolutionary terms, at least), so Martin et al. (2010) speculated that the allele for dry earwax may have increased because people with less body odor have better mating success, and therefore have more offspring. This would be difficult to test in most countries, because almost everyone has wet earwax in some places, almost everyone has dry earwax in other places, or earwax type is strongly associated with ancestry in countries with more diverse populations. But in Japan and a few other countries, people of the majority ethnic background have intermediate allele frequencies, so there are substantial numbers of both wet and dry earwax people. DNA companies like 23andMe and Ancestry.com know the ABCC11 genotype (and ancestry) of their customers, so if they asked their Japanese customers how old they were and how many children they've had, they could quickly find out if people with dry earwax have had more children in recent times. If there is a difference, the misleading clickbait headlines would write themselves--"This one weird thing about your body determines whether you'll die childless and alone!"--but it would be fascinating to find out whether variation in this one gene actually affects mating success. Of course, if there is a difference in average number of offspring between stinky people with wet earwax and odorless people with dry earwax, it's probably quite small, because the estimated difference in fitness is about 1 percent (Ohashi et al. 2011). And if there is no difference in mating success now, there may have been a difference in the past, before the invention of showers, washing machines, and deodorant.
References
Adachi, B. 1937. Das Ohrenschmalz als Rassenmerkmal und der Rassengeruch ("Achselgeruch") nebst dem Rassenunterschied der Schweissdrüsen. Zeitschrift für Rassenkunde und die Gesamte Forschung am Menschen 6: 273-307.
Beesley, J., S. E. Johnatty, X. Q. Chen, A. B. Spurdle, P. Peterlongo, M. Barile, V. Pensotti, S. Manoukian, P. Radice, and G. Chenevix-Trench. 2011. No evidence for an association between the earwax-associated polymorphism in ABCC11 and breast cancer risk in Caucasian women. Breast Cancer Research and Treatment 126: 235-239.
Hlaváč, V., R. Václavíková, V. Brynychová, R. Koževnikovová, K. Kopečková, D. Vrána, J. Gatě, and P. Souček. 2020. Role of genetic variation in ABC transporters in breast cancer prognosis and therapy response. International Journal of Molecular Science 21: 9556.
Ibraimov, A.I. 1991. Cerumen phenotypes in certain populations of Eurasia and Africa. American Journal of Physical Anthropology 84: 209-211.
Ing, R., L. Petrakis, and H. C. Ho. 1973. Evidence against association between wet cerumen and breast cancer. Lancet 1: 41.
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Lang, T., et al. (13 co-authors). 2011. The earwax-associated SNP c.538G>A (G180R) in ABCC11 is not associated with breast cancer risk in Europeans. Breast Cancer Research and Treatment, e-pub ahead of print.
Martin, A., M. Saathoff, F. Kuhn, H. Max, L. Terstegen, and A. Natsch. 2010. A functional ABCC11 allele is essential in the biochemical formation of human axillary odor. Journal of Investigative Dermatology 130: 529-540.
Matsunaga, E. 1962. The dimorphism in human normal cerumen. Annals of Human Genetics 25: 273-286.
Miura, K., K. Yoshiura, S. Miura, T. Shimada, K. Yamasaki, A. Yoshida, D. Nakayama, Y. Shibata, N. Niikawa, and H. Masuzaki. 2007. A strong association between human earwax-type and apocrine colostrum secretion from the mammary gland. Human Genetics 121: 631-633.
Nakajima, A., and I. Hirano. 1969. Distribution and inheritance of earwax types: a study on inhabitants in Awa District, Chiba Prefecture. Japanese Journal of Human Genetics 13: 201-207.
Nakano, M., N. Miwa, A. Hirano, K. Yoshiura, and N. Niikawa. 2009. A strong association of axillary osmidrosis with the wet earwax type determined by genotyping of the ABCC11 gene. BMC Genetics 10:42.
Ohashi, J., I. Naka, and N. Tsuchiya. 2011. The impact of natural selection on an ABCC11 SNP determining earwax type. Molecular Biology and Evolution 28: 849-857.
Ota, I. et al. (17 co-authors). 2010. Association between breast cancer risk and the wild-type allele of human ABC transporter ABCC11. Anticancer Research 30: 5189-5194.
Petrakis, N.L. 1971. Cerumen genetics and human breast cancer. Science 173: 347-349.
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Petrakis, N. L., V. L. Ernster, S. T. Sacks, E. B. King, R. J. Schweitzer, T. K. Hunt, M.-C. King. 1981. Epidemiology of breast secretion: Association with breast cancer risk factors and cerumen type. Journal of the National Cancer Institute 67: 277-284.
Petrakis, N.L., S. L. Wiesenfeld, and L. Flander. 1986. Possible influence of age on the expression of the heterozygous cerumen phenotype. American Journal of Physical Anthropology 69: 437-440.
Petrakis, N. L., E. B. King, M. Lee, and R. Miike. 1990. Cerumen phenotype and proliferative epithelium in breast fluids of United States-born vs. immigrant Asian women: a possible genetic-environmental interaction. Breast Cancer Research and Treatment 16: 279-285.
Ren, Y., W. Liu, J. Chen, J. Wang, K. Wang, J. Zhou, S. Cai, M. Zheng, J. Liu, L. Liu, and D. Xue. 2017. A missense variant of the ABCC11 gene is associated with axillary osmidrosis susceptibility and clinical phenotypes in the Chinese Han population. Scientific Reports 7: 46355.
Rodriguez, S., C.D. Steer, A. Farrow, J. Golding, and I.N.M. Day. 2013. Dependence of deodorant usage on ABCC11 genotype: Scope for personalized genetics in personal hygiene. Journal of Investigative Dermatology 133: 1760-1767.
Tomita, H., K. Yamada, M. Ghadami, T. Ogura, Y. Yanai, K. Nakatomi, M. Sadamatsu, A. Masui, N. Kato, and N. Niikawa. 2002. Mapping of the wet/dry earwax locus to the pericentromeric region of chromosome 16. Lancet 359: 2000-2002.
Toyoda, Y., et al. (12 co-authors). 2009. Earwax, osmidrosis, and breast cancer: why does one SNP (538 G>A) in the human ABC transporter ABCC11 gene determine earwax type? FASEB Journal 23:2001-2013.
Toyoda, Y., T. Takada, T. Gomi, H. Nakagawa, T. Ishikawa, and H. Suzuki. 2017. Clinical and molecular evidence of ABCC!! protein expression in axillary apocrine glands of patients with axillary osmidrosis. International Journal of Molecular Sciences 18:417.
Yoo, W. M., N. S. Pae, S. J. Lee, T. S. Roh, S. Chung, and K. C. Tark. 2006. Endoscopy-assisted ultrasonic surgical aspiration of axillary osmidrosis: a retrospective review of 896 consecutive patients from 1998 to 2004. Journal of Plastic, Reconstructive and Aesthetic Surgery 59: 978-982.
Yoshiura, K., et al. (39 co-authors). 2006. A SNP in the ABCC11 gene is the determinant of human earwax type. Nature Genetics 38: 324-330.
OMIM entry on earwax and OMIM entry on ABCC11
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This page was last revised October 26, 2026. ©2026 by John H. McDonald. Content is available under the Creative Commons Attribution-Noncommercial license.