Cauliflower Glucosinolates: Sinigrin, Indoles and the Sulforaphane Question

If you have read anything about cruciferous vegetables you have read about sulforaphane, and you have probably assumed cauliflower is a sulforaphane vegetable. It is not, really — that is broccoli's story, and broccoli sprouts' more than broccoli's. Cauliflower carries a different mix of the same family of compounds: it is led by sinigrin, the mustard-oil glucosinolate that also flavours horseradish and brown mustard, alongside glucoiberin and a healthy share of the indole glucosinolates glucobrassicin and neoglucobrassicin. That difference is not a demotion. It means cauliflower delivers allyl isothiocyanate and indole-3-carbinol where broccoli delivers sulforaphane, and those compounds do overlapping but not identical things. This page explains what is actually in a cauliflower head, what your body does with it, how much survives the pan, and how to cook so that most of it reaches you.

Table of Contents

  1. What a Glucosinolate Actually Is
  2. Cauliflower's Own Profile
  3. The Sulforaphane Question, Answered Honestly
  4. Myrosinase: the Enzyme That Has to Survive
  5. Indole-3-Carbinol and DIM
  6. What the Human Evidence Shows
  7. Your Genes Change the Answer
  8. Boiling, Steaming, Roasting and Raw
  9. Storage, Freezing and the Supermarket Question
  10. Getting the Most From a Head of Cauliflower
  11. Key Research Papers
  12. Connections
  13. Featured Videos

What a Glucosinolate Actually Is

A glucosinolate is a storage molecule. It is a sugar joined to a sulfur atom joined to a side chain, and in an intact plant cell it is completely inert — no smell, no taste, no biological activity worth mentioning. The plant keeps thousands of these molecules dissolved in its cell fluid, and it keeps the enzyme that activates them, myrosinase, locked away in separate cells called myrosin cells. Two loaded halves of a weapon, stored apart.

Damage the tissue — a caterpillar's jaws, your knife, your teeth — and the two compartments break open together. Myrosinase strips the sugar off the glucosinolate, and the unstable fragment that remains rearranges within seconds into an isothiocyanate: a small, sharp, volatile molecule. That reaction is the entire point. Isothiocyanates are what make mustard hot, horseradish painful, wasabi sinus-clearing, and cauliflower faintly, pleasantly sulfurous. The plant is not producing them for your benefit; it is producing a chemical defence at the exact moment it is being eaten.

Fahey, Zalcmann and Talalay catalogued the family in 2001 and found well over a hundred distinct glucosinolates distributed across the mustard order, each with its own side chain and therefore its own isothiocyanate. The side chain determines everything downstream: how pungent it is, how fast it is absorbed, which enzymes it induces in your cells, and how quickly your liver disposes of it. This is why "cruciferous vegetables are good for you" is a true but lazy statement. Broccoli, cauliflower, cabbage, Brussels sprouts, kale, watercress and mustard greens are all delivering glucosinolates, but they are delivering different ones.

One more piece of the machinery matters for cooking. Alongside myrosinase, brassicas carry a protein called the epithiospecifier protein (ESP). When ESP is active, it hijacks the breakdown reaction and steers it away from isothiocyanates toward nitriles — compounds with much weaker biological activity. ESP is more heat-sensitive than myrosinase is. That single fact is the reason gentle cooking can beat raw, and it comes back in the cooking section below.

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Cauliflower's Own Profile

The reference survey here is Kushad and colleagues' 1999 analysis, which measured glucosinolate content across a large collection of Brassica oleracea crops — broccoli, cauliflower, cabbage, Brussels sprouts and kale — using the same method on all of them, which is what makes the comparison meaningful. Two things came out of it that matter for cauliflower.

First, the crops differ by which glucosinolate dominates, not just by how much they have. Broccoli's profile is led by glucoraphanin, the precursor of sulforaphane. Cauliflower's is led by sinigrin and glucoiberin — aliphatic glucosinolates that break down to allyl isothiocyanate and iberin respectively. Cauliflower does contain glucoraphanin, but typically at levels well below broccoli's, and far below broccoli sprouts', which can carry many times the concentration of the mature vegetable.

Second, the variation within a crop is enormous. Kushad's collection showed order-of-magnitude differences between cultivars of the same vegetable. Add in growing conditions — sulfur availability in the soil, temperature, water stress, how long the head sat in a truck — and any single number you read for "the glucosinolate content of cauliflower" is a snapshot of one sample, not a property of the vegetable. This is the honest reason nutrition labels do not carry glucosinolate figures.

Cauliflower's practical line-up looks roughly like this:

  1. Sinigrin (allyl glucosinolate) → allyl isothiocyanate. The mustard-oil compound. It is the sharpest-tasting of the group and the one most responsible for the faint bite of raw cauliflower and the pungent note of an overcooked one. Allyl isothiocyanate is well studied as an inducer of phase II detoxification enzymes and as an antimicrobial.
  2. Glucoiberin → iberin. Chemically a close cousin of sulforaphane — same sulfinyl group, one carbon shorter in the chain — and it activates the same Nrf2 antioxidant-response pathway, though it has been studied far less.
  3. Glucobrassicin and neoglucobrassicin (indole glucosinolates) → indole-3-carbinol and related indoles. Cauliflower is a solid source of these. They behave completely differently from the isothiocyanates and get their own section below.
  4. Glucoraphanin → sulforaphane. Present, real, and modest.

One clarification worth making because it trips people up: the white curd is not the only part with glucosinolates. The leaves and the thick stem that most people throw away carry them too, often in higher concentration than the florets. If you want more of this chemistry per head, stop discarding two-thirds of the plant — the stem sliced thin is excellent roasted, and the outer leaves roast like kale.

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The Sulforaphane Question, Answered Honestly

Sulforaphane has the best evidence base of any compound in this family, and it deserves it. Fahey and colleagues' work on broccoli sprouts established that a young sprout can carry many times the glucoraphanin of a mature head, and Egner's randomised trial in Jiangsu, China, showed that a broccoli sprout beverage measurably accelerated the urinary excretion of airborne pollutants in people breathing heavily polluted air — a rare case of a food-derived compound producing a clean, quantifiable human biomarker result.

None of that is a cauliflower result. If your specific goal is sulforaphane, the honest ranking is broccoli sprouts > broccoli > cauliflower, and it is not close. Buying cauliflower to get sulforaphane is like buying white bread to get fibre — there is some in there, but you have picked the wrong food for the job.

What is also true, and gets lost in the sulforaphane enthusiasm, is that the human epidemiology was never built on sulforaphane. The cohort studies that link cruciferous vegetables to lower cancer and cardiovascular mortality asked people how many servings of cruciferous vegetables they ate, not how much glucoraphanin they consumed. Cauliflower counted in those servings. The population-level signal comes from the whole family, and the mechanistic explanation is plural: isothiocyanates of several kinds inducing phase II enzymes, indoles acting on hormone metabolism and cell-cycle control, plus the fibre, folate, vitamin C and potassium that come attached to any of these vegetables.

So the fair summary is: cauliflower is a good cruciferous vegetable and a poor sulforaphane source. Eat it for the first reason. If you want the second, add broccoli or grow sprouts, and read our Sulforaphane page and Cabbage's glucosinolate deep-dive, which covers the shared chemistry of the family in more detail than we repeat here.

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Myrosinase: the Enzyme That Has to Survive

Everything above depends on one fragile protein. Myrosinase is an ordinary plant enzyme, and like most enzymes it denatures with heat. Take cauliflower past roughly the temperature of a hard simmer for more than a few minutes and the myrosinase is gone. The glucosinolates are still there — they are heat-stable enough to survive normal cooking reasonably well — but nothing is left to convert them.

That is not the end of the road, because your gut bacteria also carry myrosinase-like activity. Colonic bacteria will hydrolyse a portion of intact glucosinolates that reach the large intestine, and isothiocyanates do appear in urine after fully cooked cruciferous meals. But bacterial conversion is inefficient, highly variable between people, and it happens far down the gut rather than in the small intestine where absorption is best.

Two human studies put a number on the gap. Conaway and colleagues compared fresh and steamed broccoli in volunteers and found substantially greater isothiocyanate recovery from the fresh vegetable. Vermeulen and colleagues ran a crossover study of raw versus fully cooked broccoli and found sulforaphane bioavailability roughly ten times higher from the raw vegetable — the difference between converting a third of what you ate and converting a few percent of it. Cauliflower has not been measured to the same depth, but the enzyme is the same enzyme and there is no reason to expect a different pattern.

The practical consequences are large and easy to act on, and they are collected in the practical section below. The headline one: chop the cauliflower and let it sit before it meets heat. Cutting starts the myrosinase reaction; giving it about forty minutes on the board lets the enzyme finish its work while it is still alive, so that by the time the pan destroys it the isothiocyanates have already been made. This "chop and hold" trick has been demonstrated for broccoli and rests on chemistry that applies to the whole family.

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Indole-3-Carbinol and DIM

Cauliflower's indole glucosinolates — glucobrassicin and neoglucobrassicin — take a different route. Myrosinase releases indole-3-carbinol (I3C), which is unstable in acid. In the stomach it condenses with itself, forming 3,3'-diindolylmethane (DIM) and a family of larger oligomers. So what your bloodstream actually sees after a plate of cauliflower is not I3C but its acid-condensation products, chiefly DIM.

These compounds act on cell signalling rather than on antioxidant defences. Firestone and Bjeldanes reviewed the antiproliferative pathways: in cell and animal models, I3C and DIM slow the cell cycle, affect apoptosis regulators, and interact with the aryl hydrocarbon receptor — the same receptor that senses certain environmental pollutants and switches on drug-metabolising enzymes. They also influence oestrogen metabolism, shifting the balance of hydroxylated oestrogen metabolites, which is the origin of the long-standing interest in cruciferous vegetables and hormone-related cancers.

Two honest cautions belong with this, because the supplement market is loud about I3C and DIM:

  1. Supplement doses are not food doses. A capsule can contain more I3C or DIM than a week of cauliflower. Nearly all the mechanistic work uses concentrations reachable by supplementation, not by dinner. Extrapolating the cell-culture findings to "eat more cauliflower and this will happen to you" is not supported, and we will not pretend otherwise.
  2. Aryl hydrocarbon receptor activity means drug-interaction potential. Compounds that induce cytochrome P450 enzymes can change how fast the liver clears medications. At food intakes this is a non-issue for essentially everyone. At sustained high supplement doses it is a real consideration and worth raising with whoever prescribes your medicines.

The reasonable position is the one the epidemiology supports: eat cruciferous vegetables regularly, in food amounts, as part of a varied diet. Cauliflower's contribution to that is genuine, and its indole content is one of the places it holds its own against broccoli rather than trailing it.

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What the Human Evidence Shows

Step back from the molecules and ask what happens to people who eat these vegetables. The answer is consistent in direction, modest in size, and observational in nature — which is exactly how it should be described.

Cancer. Higdon, Delage, Williams and Dashwood's 2007 review remains the clearest account of the field: the epidemiological evidence for cruciferous vegetables and cancer risk is suggestive rather than conclusive, stronger for some cancers than others, and complicated by the difficulty of measuring intake accurately in a food-frequency questionnaire. Two meta-analyses of colorectal cancer — Wu and colleagues in Annals of Oncology and Tse and Eslick in Nutrition and Cancer — both found lower risk in the highest-intake groups, with the size of the association depending heavily on which studies were pooled and how intake was categorised.

Total and cardiovascular mortality. Zhang and colleagues examined cruciferous vegetable consumption in large Shanghai cohorts and found it associated with lower total and cardiovascular mortality. Observational again, and confounded by everything that travels with eating vegetables — but the direction has been reproduced in several populations.

What none of this can do is separate cauliflower from the family. No cohort has enough cauliflower-specific data to isolate it, and no trial has randomised people to cauliflower for long enough to measure a hard outcome. That is a limitation of the evidence, not a criticism of the vegetable, and it applies equally to broccoli and cabbage.

The trials that do exist measure biomarkers over weeks, not disease over decades: enzyme induction, detoxification markers, oxidative stress markers, urinary metabolite excretion. Egner's broccoli sprout trial is the cleanest of them. They establish that the mechanism is real in humans. They do not establish how much disease it prevents.

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Your Genes Change the Answer

Isothiocyanates are cleared from the body by conjugation with glutathione, a reaction run by the glutathione S-transferase enzymes. Two of those genes, GSTM1 and GSTT1, are commonly deleted — a large fraction of people carry no working copy of one or both, and the frequency varies substantially between populations.

Lampe and Peterson laid out what this means. People who lack the enzyme clear isothiocyanates more slowly, so the compounds linger longer at higher concentrations. Counter-intuitively, several studies have found the protective association between cruciferous intake and cancer risk to be stronger in the null genotypes — consistent with longer exposure producing more enzyme induction. Other studies have found the opposite or nothing at all.

The honest reading is that genotype is one reason the epidemiology is noisy: a single dietary exposure may genuinely do different things in different people, and studies that pool everyone together will average a real effect toward zero. It is not a reason to get tested. There is no clinical recommendation attached to a GSTM1 result, and the dietary advice does not change: eat the vegetables.

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Boiling, Steaming, Roasting and Raw

This is where the science becomes genuinely actionable, because the differences between cooking methods are large.

Boiling is the worst option, and the reason is leaching, not heat. Song and Thornalley measured glucosinolate content in brassica vegetables through storage, processing and cooking, and found that boiling produced by far the largest losses — the water-soluble glucosinolates simply dissolve out of the vegetable and into the pan. Steaming, microwaving and stir-frying caused little loss by comparison. Pellegrini and colleagues compared boiling, steaming and microwaving across raw and frozen brassicas including cauliflower and reached a compatible conclusion.

Two corollaries follow. If you boil, use the water — keep it for a soup or a sauce and you recover most of what leached out. And if you boil, do it briefly in a small amount of water rather than at length in a large pot; both time and water volume drive the loss.

Steaming is the best all-round method. It cannot leach, because the vegetable never sits in water, and Rungapamestry's review of cooking and glucosinolate fate makes the further point that mild heating can actually increase isothiocyanate yield. Recall the epithiospecifier protein, which diverts breakdown to inactive nitriles: ESP denatures at a lower temperature than myrosinase does. A short, gentle steam — on the order of a few minutes, to the point where a knife tip meets slight resistance — can knock out ESP while leaving enough myrosinase alive to work. Steam it to collapse and you lose both.

Roasting is better than its reputation. Dry heat means nothing leaches, and the browning that makes roasted cauliflower delicious is Maillard chemistry that has nothing to do with glucosinolates. Temperatures are higher, so some thermal degradation occurs, but for retention roasting comfortably beats a long boil. It is also the method most likely to get cauliflower actually eaten, which counts for more than a percentage point of glucosinolate retention.

Raw is chemically optimal and gastrointestinally demanding. Full myrosinase activity, no thermal loss, no leaching — and, for a sizeable minority of people, an evening of gas and bloating, because raw cruciferous fibre and cauliflower's mannitol content are exactly what a sensitive gut struggles with. Our FODMAPs and tolerance page covers that in full. If raw cauliflower suits you, it is the most efficient way to eat it. If it does not, cooked cauliflower you actually enjoy beats raw cauliflower you avoid.

Cauliflower-specific data is thinner than broccoli-specific data, but it exists. Girgin and El measured how cooking changed sinigrin bioaccessibility, phenolic content and antimutagenic activity in cauliflower itself — one of the few studies to use this vegetable rather than extrapolate from its relatives — and Ahmed and Ali examined bioactive compounds and antioxidant activity in fresh and processed white cauliflower. Both confirm that processing method matters materially for what ends up available to you.

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Storage, Freezing and the Supermarket Question

Glucosinolates decline in storage. Song and Thornalley's work covered the whole supply chain, and Verkerk's review made the same point at greater length: intake is determined not only by what the plant produced but by everything that happened between the field and your fork — days in transit, days in a display case, days in your fridge.

A practical translation: buy a head that looks like it was picked recently. Tight, heavy, cream-white curd with no grey speckling, and green leaves that are still crisp rather than yellowing and rubbery. The leaves are the honest indicator, because they wilt visibly before the curd does. Store it whole and unwashed in the fridge and cut it when you cook it; cut surfaces both dry out and start their myrosinase reaction on the counter rather than on your plate.

Frozen cauliflower is a real trade-off, and it is worth understanding rather than guessing. Commercial freezing requires blanching — a brief scald that inactivates the enzymes which would otherwise cause off-flavours in the freezer. Blanching does not just inactivate spoilage enzymes; it inactivates myrosinase too. So frozen cauliflower arrives with its glucosinolates largely intact but its activating enzyme dead, which means conversion depends almost entirely on your gut bacteria. Volden and colleagues measured glucosinolates, ascorbic acid, phenols and anthocyanins in cauliflower through long-term freezer storage and documented the losses in detail.

The fix costs nothing: add a source of external myrosinase to cooked or frozen cauliflower. Mustard seed, mustard powder, horseradish, wasabi and rocket all carry active myrosinase. Okunade and colleagues demonstrated directly that adding mustard seeds to heat-processed brassica increased sulforaphane bioavailability. A teaspoon of whole-grain mustard stirred into cauliflower cheese, or a grating of horseradish over a roasted head, is a genuine chemical intervention that also happens to taste good.

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Getting the Most From a Head of Cauliflower

Everything above condenses into a short list. None of it is fussy, and none of it requires buying anything.

  1. Chop, then wait. Break the head into florets, then leave it on the board for about forty minutes before it meets heat. This is the single highest-value habit on the list — it lets the plant's own enzyme finish the job while it is still alive.
  2. Steam briefly rather than boil. A few minutes, to just-tender. If you boil, keep the water for soup.
  3. Roast when you want it eaten. High heat, dry, until the edges catch. Retention is good and enthusiasm is better.
  4. Eat some of it raw. Thin-sliced raw cauliflower in a salad, or grated raw as a slaw, gives you full enzyme activity. Start small if your gut is sensitive.
  5. Add mustard, horseradish or wasabi to cooked cauliflower. External myrosinase restores the conversion that heat destroyed. Whole-grain mustard in a cheese sauce; horseradish over a roasted head; a mustard vinaigrette on a warm salad.
  6. Use the stem and the leaves. They carry glucosinolates too and most people bin them. Slice the stem thin and roast it with the florets; roast the outer leaves like kale chips.
  7. Vary the family. Cauliflower for sinigrin and indoles, broccoli for glucoraphanin, watercress for phenethyl isothiocyanate, cabbage for volume and cost. The evidence is for the family, so eat the family.
  8. Buy fresh-looking heads and use them within a few days. Crisp green leaves are the tell.
  9. Do not chase this with supplements. Nothing in the human evidence supports replacing the vegetable with an I3C or DIM capsule, and capsules bring interaction potential that food does not.

A realistic target is a few servings of cruciferous vegetables a week, of which cauliflower can be one or two. There is no threshold dose in the literature to hit and no benefit in forcing down more than you enjoy.

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Key Research Papers

  1. Fahey JW, Zalcmann AT, Talalay P. The chemical diversity and distribution of glucosinolates and isothiocyanates among plants. Phytochemistry. 2001;56(1):5-51. — doi:10.1016/S0031-9422(00)00316-2
  2. Kushad MM, Brown AF, Kurilich AC, et al. Variation of glucosinolates in vegetable crops of Brassica oleracea. Journal of Agricultural and Food Chemistry. 1999;47(4):1541-1548. — doi:10.1021/jf980985s
  3. Song L, Thornalley PJ. Effect of storage, processing and cooking on glucosinolate content of Brassica vegetables. Food and Chemical Toxicology. 2007;45(2):216-224. — doi:10.1016/j.fct.2006.07.021
  4. Verkerk R, Schreiner M, Krumbein A, et al. Glucosinolates in Brassica vegetables: the influence of the food supply chain on intake, bioavailability and human health. Molecular Nutrition & Food Research. 2009;53(S2):S219-S265. — doi:10.1002/mnfr.200800065
  5. Rungapamestry V, Duncan AJ, Fuller Z, Ratcliffe B. Effect of cooking brassica vegetables on the subsequent hydrolysis and metabolic fate of glucosinolates. Proceedings of the Nutrition Society. 2007;66(1):69-81. — doi:10.1017/S0029665107005319
  6. Vermeulen M, Klopping-Ketelaars IWAA, van den Berg R, Vaes WHJ. Bioavailability and kinetics of sulforaphane in humans after consumption of cooked versus raw broccoli. Journal of Agricultural and Food Chemistry. 2008;56(22):10505-10509. — doi:10.1021/jf801989e
  7. Conaway CC, Getahun SM, Liebes LL, et al. Disposition of glucosinolates and sulforaphane in humans after ingestion of steamed and fresh broccoli. Nutrition and Cancer. 2000;38(2):168-178. — doi:10.1207/S15327914NC382_5
  8. Okunade O, Niranjan K, Ghawi SK, Kuhnle G, Methven L. Supplementation of the diet by exogenous myrosinase via mustard seeds to increase the bioavailability of sulforaphane in healthy human subjects after the consumption of cooked broccoli. Molecular Nutrition & Food Research. 2018;62(18):1700980. — doi:10.1002/mnfr.201700980
  9. Girgin N, El SN. Effects of cooking on in vitro sinigrin bioaccessibility, total phenols, antioxidant and antimutagenic activity of cauliflower (Brassica oleraceae L. var. Botrytis). Journal of Food Composition and Analysis. 2015;37:119-127. — doi:10.1016/j.jfca.2014.04.013
  10. Ahmed FA, Ali RFM. Bioactive compounds and antioxidant activity of fresh and processed white cauliflower. BioMed Research International. 2013;2013:367819. — doi:10.1155/2013/367819
  11. Volden J, Bengtsson GB, Wicklund T. Glucosinolates, L-ascorbic acid, total phenols, anthocyanins, antioxidant capacities and colour in cauliflower (Brassica oleracea L. ssp. botrytis): effects of long-term freezer storage. Food Chemistry. 2009;112(4):967-976. — doi:10.1016/j.foodchem.2008.07.018
  12. Pellegrini N, Chiavaro E, Gardana C, et al. Effect of different cooking methods on color, phytochemical concentration, and antioxidant capacity of raw and frozen brassica vegetables. Journal of Agricultural and Food Chemistry. 2010;58(7):4310-4321. — doi:10.1021/jf904306r
  13. Higdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacological Research. 2007;55(3):224-236. — doi:10.1016/j.phrs.2007.01.009
  14. Wu QJ, Yang Y, Vogtmann E, et al. Cruciferous vegetables intake and the risk of colorectal cancer: a meta-analysis of observational studies. Annals of Oncology. 2013;24(4):1079-1087. — doi:10.1093/annonc/mds601
  15. Tse G, Eslick GD. Cruciferous vegetables and risk of colorectal neoplasms: a systematic review and meta-analysis. Nutrition and Cancer. 2014;66(1):128-139. — doi:10.1080/01635581.2014.852686
  16. Zhang X, Shu XO, Xiang YB, et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality. The American Journal of Clinical Nutrition. 2011;94(1):240-246. — doi:10.3945/ajcn.110.009340
  17. Lampe JW, Peterson S. Brassica, biotransformation and cancer risk: genetic polymorphisms alter the preventive effects of cruciferous vegetables. The Journal of Nutrition. 2002;132(10):2991-2994. — doi:10.1093/jn/131.10.2991
  18. Firestone GL, Bjeldanes LF. Indole-3-carbinol and 3-3'-diindolylmethane antiproliferative signaling pathways control cell-cycle gene transcription in human breast cancer cells by regulating promoter-Sp1 transcription factor interactions. The Journal of Nutrition. 2003;133(7):2448S-2455S. — doi:10.1093/jn/133.7.2448S
  19. Egner PA, Chen JG, Zarth AT, et al. Rapid and sustainable detoxication of airborne pollutants by broccoli sprout beverage: results of a randomized clinical trial in China. Cancer Prevention Research. 2014;7(8):813-823. — doi:10.1158/1940-6207.CAPR-14-0103

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