It's somewhat simplistic view that dopamine is directly proportional with pleasure. This was a mainstream hypothesis in the 1980s, but has fallen out of favor:
The idea that dopamine was a mechanism for pleasure is known as the ‘dopamine hedonia’ or ‘dopamine pleasure’ hypothesis, and was originally proposed by Roy Wise: “dopamine junctions represent a synaptic way station…where sensory inputs are translated into the hedonic messages we experience as pleasure, euphoria or ‘yumminess’.”(Wise, 1980) (p. 94). Conversely, the ‘dopamine pleasure hypothesis’ postulated that reduction of dopamine neurotransmission caused loss of pleasure. This inverse hypothesis is known as the ‘dopamine anhedonia hypothesis’ (Ettenberg and McFarland, 2003; Hnasko et al., 2006; Smith, 1995; Wise and Colle, 1984; Wise et al., 1978).
However, today relatively few neuroscientists who study dopamine in reward appear to assert in print that dopamine causes pleasure. Even original proponents are no longer so enthusiastic. For example, by the mid-1990s Wise had retracted the dopamine hedonia hypothesis: he was quoted to say “I no longer believe that the amount of pleasure felt is proportional to the amount of dopamine floating around in the brain” (p.35) (Wickelgren, 1997), and more recently concluded that “pleasure is not a necessary correlate of dopamine elevations” (p.179)(Wise, 2008).
The reason for this change in perspective are observations like
for human ratings of subjective pleasure, Parkinson’s patients who have extensive dopamine depletion due to their disease still give normal hedonic ratings of liking to the sensory pleasure of a sweet taste (Meyers et al., 2010; Sienkiewicz-Jarosz et al., 2013). And human subjective ratings of drug pleasure (e.g., cocaine) are not reduced by pharmacological disruption of dopamine systems, even when dopamine suppression does reduce wanting ratings (Brauer and De Wit, 1997; Leyton et al., 2007)
Related questions have arisen recently about whether other types of clinical 'anhedonia' truly live up to their lack-of-pleasure label, such as in depression or of schizophrenia. Closer inspection has suggested that many patients with conditions may not be anhedonic any more than Parkinson’s patients: at least sensory pleasures may persist virtually intact (Barch et al., 2014; Dowd and Barch, 2010; Sienkiewicz-Jarosz et al., 2005; Treadway and Zald, 2011). This has given rise in some cases to a reinterpretation of anhedonia as ‘avolition’ or more specific impairment of incentive motivation.
Conversely, dopamine stimulations do not reliably cause pleasure. Dopamine elevations in NAc fail to enhance ‘liking’ for sweetness, despite increasing motivational ‘wanting’ to obtain the same rewards (e.g., higher runway performance of hyper-dopaminergic mutant mice; higher peaks of cue-triggered effort to obtain sucrose reward, increases in reward consumption, and higher peaks of neural firing in NAc-VP circuits that encode cue-triggered ‘wanting’)(Pecina and Berridge, 2013; Peciña et al., 2003; Smith et al., 2011; Wyvell and Berridge, 2000). In people, L-DOPA-evoked surges in brain dopamine levels do not increase subjective pleasure ratings (Liggins et al., 2012). The intensity of dopamine NAc surges even when evoked by addictive drugs (e.g., amphetamine) correlates rather poorly with subjective liking ratings - but correlates much better with wanting ratings (Evans et al., 2006; Leyton et al., 2002). Examples of ‘wanting’-without-‘liking’ induced by dopamine stimulation also come from compulsive motivations induced in Parkinson’s patients treated with high-doses of dopamine agonists, especially direct D2/D3 receptor agonists (O'Sullivan et al., 2009). Those intense motivations range from gambling to shopping, pornography, internet, hobbies, addictive drugs, or taking excessive medication in addictive fashion (Callesen et al., 2013; Friedman and Chang, 2013; Ondo and Lai, 2008; Politis et al., 2013). Yet these cases typically do not report intense pleasure.
Another puzzle has been that if dopamine does not cause sensory pleasure, why are dopamine-promoting drugs such as cocaine or methamphetamine so pleasant? [...]
A neural explanation for why cocaine is pleasant may be that cocaine and amphetamine also stimulate secondary recruitment of endogenous opioid and related neurobiological hedonic mechanisms, beyond directly raising dopamine release. Those recruited secondary mechanisms may more directly cause ‘liking’ reactions and subjective pleasure. For instance, dopamine-stimulating drugs recruit elevation in nucleus accumbens of endogenous opioid and GABA signals (Colasanti et al., 2012; Soderman and Unterwald, 2009; Tritsch et al., 2012). Elevated endogenous opioid release in a site such as the NAc hedonic hotspot could amplify ‘liking’ as described above, resulting in a more genuinely pleasurable experience. Similarly, GABA signals in the far rostral strip of NAc shell can also enhance true ‘liking’ (Faure et al., 2010), which could occur if drugs of abuse that stimulate dopamine neurons also stimulate some of those neurons to co-release more GABA in NAc (Tritsch et al., 2012).
However, hedonic effects might well change over time. As a drug was taken repeatedly, mesolimbic dopaminergic sensitization could consequently occur in susceptible individuals to amplify ‘wanting’ (Leyton and Vezina, 2013; Lodge and Grace, 2011; Wolf and Ferrario, 2010), even if opioid hedonic mechanisms underwent down-regulation due to continual drug stimulation, producing ‘liking’ tolerance. Incentive-sensitization would produce addiction, by selectively magnifying cue-triggered ‘wanting’ to take the drug again, and so powerfully cause motivation even if the drug became less pleasant (Robinson and Berridge, 1993).
In simple words, there are competing hypotheses how addiction relates to pleasure, i.e. more dopamine = more pleasure/euphoria = more addiction as in the PBS quote may not be how it works.
The review paper also has a very interesting section on the (direct brain) "pleasure electrode" research (electrodes places "along the mesolimbic path, where electrodes can elicit surges in NAc dopamine release"), research which is also rather mixed, but it's too long to quote here given that it's more tangential to the claim in question. As my summary of that, older research was put in question by newer findings that e.g. patients on deep brain stimulation on that pathway (typically also Parkinson patients) develop various enhanced "wants" (as they do on Parkinson medication) but often enough they are even unaware of any electrical stimulation going on, i.e. they don't experience pleasure from the stimulation itself may not even sense the stimulation. (Somewhat creepy finding for the tinfoil hats of "mind control", I have to say.)
One would also expect to find at least an innate (i.e. not caused directly by the drug but e.g. by the anticipation to it) dopamine response to opioid administration in opioid addicts. Alas, while one is found in animal models (and it's less than for psychostimulants), in vivo studies in humans seem to have failed to show it insofar (see a 2008 primary study on that and a 2015 review that mentions no other), despite the fact that subjective feelings of rush/high in response to opioids are easy to find (even with statistical significance) in humans, even more so in addicts as shown e.g. in that 2008 primary study. (This might be because such self-generated as opposed to drug-induced dopamine response is also sensitive to the experimental conditions, i.e. what the subjects are told to expect might happen, as another study found.)
Now as far as pleasure rankings go, I don't know if (and seriously doubt that) anyone has managed to actually compare "likes" for that many diverse experiences and substances in terms of their pleasure intensity (as the 2M-views youtube video shows), due to the methodological challenges involved.
Just to hint how difficult that may be study, even considering the peak dopamine response as a measure of "want" (instead of "like") and thus using peak dopamine as a measure of potential for addiction, there are/were some other experimental factors involved, chiefly the timing of the dopamine spike.
One fairly cited (2007) animal study found that--given a mutually exclusive choice-- rats overwhelmingly preferred saccharin (a calories-free artificial sweetener) to cocaine, at least on a behavioral level in terms of the number of "hits" they took. The most interesting bit of that study it that it managed to get cocaine-addicted rats to switch to saccharin. That finding has since been replicated with heroin as well, i.e. sweetener is preferred even over heroin in similar experiments. But that line of research ignored the timing (pharmacokinetics) of the dopamine spike involved in the reward, which comes faster with sweeteners. A 2020 study found that introducing a time delay to the sweetener reward that matches the intrinsic delay of the cocaine dopamine spike makes rats prefer cocaine over the sweetener.